Category: 827-61-2

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Optically active 3 – the preparation method of the quinine is mellow (by machine translation)

The invention relates to a method for synthesizing intermediate, which belongs to the field of organic synthesis. In particular to a simple operation, low cost, and is suitable for industrial production of optically active 3 – the preparation method of the quinine is mellow. In order to 4 – piperidine carboxylic acid as the starting material, through esterification, pro-nuclear substituted, Dieckmann condensation, decarboxylation, salt, reduction, acetylation, chemically so as to obtain the intermediate optically active 3 – the quinine is mellow. The above reaction equation is as follows: (by machine translation)

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Quinuclidine – Wikipedia,
Quinuclidine | C7H35N | ChemSpider

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Muscarinic effects on cellular functions in cultured human ciliary muscle cells

Purpose. To characterize the pharmacology of the carbachol-induced changes of phospholipase C (PLC) activity and intracellular calcium concentration ([Ca2+](i)) in cultured human ciliary muscle cells. Methods. Changes in PLC activity of cultured human ciliary muscle cells were determined by production of inositol phosphates. Single-cell dynamic fluorescence ratio imaging was used to determine [Ca2+](i). Results. Carbachol, oxotremorine-M, aceclidine, and pilocarpine stimulated PLC with mean EC50s of 20, 8, 17, and 2 muM, respectively. The effect of carbachol on PLC was partially suppressed by extracellular Ca2+ depletion. This muscarinic effect was blocked by muscarinic antagonists, such as atropine (apparent pK(i) = 9.12, nonselective for muscarinic receptor subtypes), pirenzepine (pK(i) = 6.76, selective for the M1 receptor subtype), 4DAMP (pK(i) = 9.25, selective for the M1 and M3 subtypes), and fHHSiD (pK(i) = 7.77, selective for the M3 subtype). In [Ca2+](i) experiments, carbachol increased [Ca2+](i) transients in human ciliary muscle cells in a dose-dependent manner with a mean EC50 of 7 muM. 4DAMP was approximately 100 times more potent than pirenzepine in the inhibition of the carbachol-induced [Ca2+](i) increase. [Ca2+](i) oscillations were observed after carbachol stimulation and persisted after extracellular Ca2+ depletion. Conclusions. Muscarinic agonists activate PLC and increase [Ca2+](i) in cultured human ciliary muscle cells through an M3-like muscarinic receptor subtype.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H71N | ChemSpider

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New Strategies for the Transition-Metal Catalyzed Synthesis of Aliphatic Amines

Transition-metal catalyzed reactions that are able to construct complex aliphatic amines from simple, readily available feedstocks have become a cornerstone of modern synthetic organic chemistry. In light of the ever-increasing importance of aliphatic amines across the range of chemical sciences, this review aims to provide a concise overview of modern transition-metal catalyzed approaches to alkylamine synthesis and their functionalization. Selected examples of amine bond forming reactions include: (a) hydroamination and hydroaminoalkylation, (b) transition-metal catalyzed C(sp3)-H functionalization, and (c) transition-metal catalyzed visible-light-mediated light photoredox catalysis.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H86N | ChemSpider

827-61-2, Name is Quinuclidin-3-yl acetate, belongs to quinuclidine compound, is a common compound. SDS of cas: 827-61-2In an article, once mentioned the new application about 827-61-2.

Synthesis of the optical isomers of a new anticholinergic drug, penehyclidine hydrochloride (8018)

A practical diastereoselective synthetic method for 8018 enantiopure isomers is described. The intramolecular asymmetric epoxidation of mono-sulfonate 4 was applied for the execution of the synthesis of the key chiral building block for the first time. The isomers were obtained with 70-76% yields in 99-100% ee.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H60N | ChemSpider

In heterogeneous catalysis, the catalyst is in a different phase from the reactants. Formula: C9H15NO2, At least one of the reactants interacts with the solid surface in a physical process called adsorption in such a way. 827-61-2, name is Quinuclidin-3-yl acetate. In an article£¬Which mentioned a new discovery about 827-61-2

Nonaqueous fluorinated drug delivery suspensions

Nonaqueous pharmaceutical compositions for use in aqueous physiological systems are disclosed comprising drug delivery suspension of nonaqueous perfluorocarbon or fluorinated silicone liquid carriers. The suspended drug may be water labile or water stable and therapeutic or diagnostic compounds which will remain stable and pharmaceutically effective for extended periods. The pharmaceutical compositions have improved bioavailability, are capable of low dose volume delivery, and do not degrade the incorporated therapeutic or diagnostic compounds making them well suited for multi-dose packaging and administration.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H33N | ChemSpider

One of the major reasons for studying chemical kinetics is to use measurements of the macroscopic properties of a system, Product Details of 827-61-2, such as the rate of change in the concentration of reactants or products with time.In a article, authors is Grob, Cyril A., mentioned the application of 827-61-2, Name is Quinuclidin-3-yl acetate, molecular formula is C9H15NO2

95. Inductive Charge Dispersal in Quinuclidinium Ions. Polar Effects, Part 13

Inductive charge dispersal to the alpha-, beta-, and gamma-positions of the solvated quinuclidinium ion has been examined by comparing the pKa and the derived inductivities rho1 of several 2-, 3- and 4-substituted quinuclidinium perchlorates 4, 5, and 6, respectively.The same inductivity is observed at the practically equidistant beta- and gamma-positions.It, therefore, appears that polar substituent effects are transmitted directly through the molecule.As expected, inductivity is considerably higher at the alpha-positions where through-bond and direct induction coincide.The fact that the pKa of all three series of salts correlate linearly with each other points to the common nature of these inductive electron displacements.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H59N | ChemSpider

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A practical chemoenzymatic process to access (R)-quinuclidin-3-ol on scale

(¡À)-3-Butyryloxyquinuclidinium butyrate 6 (2 M, 571 g/L), prepared from (¡À)-quinuclidin-3-ol 1 and butyric anhydride, undergoes enantioselective hydrolysis by an Aspergillus melleus protease {1.0% (w/v)} in water in the presence of Ca(OH)2 to keep the reaction at pH 7 and trap butyric acid that is introduced as part of (¡À)-6 and generated by the enzymatic hydrolysis. After a 24 h period, extraction with n-heptane provides (R)-quinuclidin-3-yl butyrate 5a, which, on methanolysis with Na2CO3, is converted into (R)-1, a common pharmacophore of neuromodulators acting on muscarinic receptors, in 96% ee and 42% overall yield from (¡À)-1. The unwanted antipode (S)-1, which is extracted into n-butanol and purified via its hydrochloride salt in 89% ee and 40% overall yield from (¡À)-1, can be racemized by the catalysis of Raney Co at 140C under an atmosphere of H2 (5 kg/cm2) to regenerate (¡À)-1 in 97% yield.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H75N | ChemSpider

Related Products of 827-61-2, A catalyst don’t appear in the overall stoichiometry of the reaction it catalyzes, but it must appear in at least one of the elementary reactions in the mechanism for the catalyzed reaction. 827-61-2, Name is Quinuclidin-3-yl acetate, molecular formula is C9H15NO2. In a Article£¬once mentioned of 827-61-2

IDrugs and idevices discovery research: Preclinical assays, techniques, and animal model studies for ocular hypotensives and neuroprotectants

Discovery ophthalmic research is centered around delineating the molecular and cellular basis of ocular diseases and finding and exploiting molecular and genetic pathways associated with them. From such studies it is possible to determine suitable intervention points to address the disease process and hopefully to discover therapeutics to treat them. An investigational new drug (IND) filing for a new small-molecule drug, peptide, antibody, genetic treatment, or a device with global health authorities requires a number of preclinical studies to provide necessary safety and efficacy data. Specific regulatory elements needed for such IND-enabling studies are beyond the scope of this article. However, to enhance the overall data packages for such entities and permit high-quality foundation-building publications for medical affairs, additional research and development studies are always desirable. This review aims to provide examples of some target localization/verification, ocular drug discovery processes, and mechanistic and portfolio-enhancing exploratory investigations for candidate drugs and devices for the treatment of ocular hypertension and glaucomatous optic neuropathy (neurodegeneration of retinal ganglion cells and their axons). Examples of compound screening assays, use of various technologies and techniques, deployment of animal models, and data obtained from such studies are also presented.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H82N | ChemSpider

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Muscarinic contraction in isolated guinea-pig trachea and antagonism by noradrenaline

In contrast to other muscarinic agonists, WAL 2014 FU does not induce bronchospasm in laboratory animals. The present investigation was intended to test the hypothesis that this is due to a particular susceptibility of the drug’s effect to antagonism by catecholamines, as a result of partial M3- agonism. The tonic activity of the muscarinic agonists, aceclidine, arecoline, carbachol, McN-A-343, RS 86, thiopilocarpine and WAL 2014 FU, was tested in groups of isolated tracheal muscle of the guinea-pig. Susceptibility to functional antagonism by beta-adrenoceptor stimulation was measured by the displacement of the concentration-force curves by 3 muM noradrenaline. Evaluation of the concentration-force relationship revealed differences in potency and intrinsic activity (carbachol=100%) ranging from 114% for arecoline to 36% for thiopilocarpine (WAL 2014 FU=63%). The catecholamine increased the concentration of agonist which induced 5% of the maximum effect achievable (EC05) values fivefold (carbachol) to more than 4,680 fold (thiopilocarpine) (WAL 2014 FU: 2,860 fold). Regression analysis between the intrinsic activity of the seven compounds and the antagonistic effect of noradrenaline revealed a significant correlation (Spearman correlation coefficient (r(s)) =-0.79; p=0,036). Inhibition of the effects of endogenous catecholamines by beta-adrenolysis with 50 muM toliprolol increased the maximal contraction induced by 1 mM WAL 2014 FU, but did not affect maximal contraction induced by 30 muM arecoline. Pretreatment with 0.3-1.0 mM dibutyrylcyclic adenosine monophosphate (DBcAMP) shifted the concentration- response curves of arecoline, WAL 2014 FU and thiopilocarpine in a similar manner to noradrenaline. The results exclude an important contribution of adenylate cyclase-coupled M2-receptors to the susceptibility of tracheal contraction by muscarinic agonists to functional antagonism by noradrenaline, but emphasize the importance of intrinsic activity at the M3-receptors. The pronounced susceptibility of WAL 2014 FU-induced contraction to functional antagonism by beta-adrenoceptor activation provides an explanation for the failure of the drug to induce bronchospasm in vivo.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H88N | ChemSpider

Synthetic Route of 827-61-2, A catalyst don’t appear in the overall stoichiometry of the reaction it catalyzes, but it must appear in at least one of the elementary reactions in the mechanism for the catalyzed reaction. 827-61-2, Name is Quinuclidin-3-yl acetate, molecular formula is C9H15NO2. In a Article£¬once mentioned of 827-61-2

Mechanism of vascular relaxation by cholinomimetic drugs with special reference to pilocarpine and arecoline

The muscarinic receptor-mediated and non-muscarinic vascular effects of cholinomimetic drugs used in glaucoma were quantified. On the isolated rat aorta, the vascular tone induced by phenylephrine is functionally antagonized by cholinomimetic drugs. Based on EC50, the relative order of potency for the endothelium-dependent vascular relaxation was acetylcholine (0.05 muM) 1 > (¡À)-methacholine (0.35 muM) 1/7 > carbachol (0.63 muM) 1/12 > (¡À)-aceclidine (1.26 muM) 1/25. The maximal effects of the four agonists varied between 82-87%. The muscarinic vascular relaxation of 0.03 muM to 100 muM pilocarpine was less than 15%. At high concentrations, pilocarpine had 1/20,000 the vascular activity of acetylcholine. Physostigmine failed to potentiate the vascular relaxation of exogenous acetylcholine, indicating the absence of acetylcholine esterase in the tissue. Arecoline, with an EC50 of 7.76 muM, was partly sensitive to the removal of the endothelium. Atropine treatment did not block the vascular effect of high concentrations of pilocarpine. Atropine, as expected, blocked the vascular effects of carbachol with KB = 3.2 nM. Pilocarpine produces vascular relaxation by its competition with spasmogens like phenylephrine, oxymetazoline, vasopressin or latanoprost. Arecoline also shares these properties with pilocarpine in the blood vessel. The molecular mechanism of the vascular effects as well as ocular clinical implications of cholinomimetic drugs is discussed.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H77N | ChemSpider