Category: 827-61-2

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Visible-Light-Mediated Metal-Free Difunctionalization of Alkenes with CO2 and Silanes or C(sp3)?H Alkanes

Catalytic alkene difunctionalization via Si?H and C?H activations represents an ideal atom- and step-economic pathway for quick assembly of molecular complexity. We herein developed a visible-light-promoted metal-free difunctionalization of alkenes using abundant CO2 and readily available Si?H and C(sp3)?H bonds as feedstocks. Through the merger of photoredox and hydrogen-atom-transfer catalysis, a variety of value-added compounds, such as beta-silacarboxylic acids and acids bearing a gamma-heteroatom (e.g., N, O, S) could be directly accessed from simple alkenes in a redox-neutral fashion.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H63N | ChemSpider

Related Products of 827-61-2, The reaction rate of a catalyzed reaction is faster than the reaction rate of the uncatalyzed reaction at the same temperature.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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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H82N | ChemSpider

Synthetic Route of 827-61-2, The reaction rate of a catalyzed reaction is faster than the reaction rate of the uncatalyzed reaction at the same temperature.827-61-2, Name is Quinuclidin-3-yl acetate, molecular formula is C9H15NO2. In a Article£¬once mentioned of 827-61-2

Metabolomics responses of Bambusa pervariabilis ¡Á Dendrocalamopsis grandis varieties to Biotic (pathogenic fungus) stress

Bambusa pervariabilis ¡Á Dendrocalamopsis grandis blight, caused by Arthrinium phaeospermum, is one of the most common and serious diseases in bamboo and occurs in the newly born twigs. Bamboo has suffered large dead areas, including more than 3000 hm2, which greatly threatens the process of returning farmlands to forests and the construction of ecological barriers. To identify differential metabolites and metabolic pathways associated with B. pervariabilis ¡Á D. grandis to A. phaeospermum, ultra-performance liquid chromatography (UPLC) and quadrupole-time of flight (Q-TOF) Mass Spectrometry (MS) combined with a data-dependent acquisition method was used to analyse the entire sample spectrum. In total, 13223 positive ion peaks and 10616 negative ion peaks were extracted. OPLS-DA and several other analyses were performed using the original data. The OPLS-DA models showed good quality and had strong predictive power, indicating clear trends in the analyses of the treatment and control groups. Clustering and KEGG pathway analyses were used to screen the differential metabolites in the treatment and control groups from the three B. pervariabilis ¡Á D. grandis varieties and reflected their metabolic responses induced by A. phaeospermum infection. The results showed that the three B. pervariabilis ¡Á D. grandis varieties mode showed significant changes in the following six resistance-related metabolites after A. phaeospermum invasion in positive and negative ion modes: proline, glutamine, dictamnine, apigenin 7-O-neohesperidoside, glutamate, and cis-Aconitate. The following four main metabolic pathways are involved: Arginine and proline metabolism, Glyoxylate and dicarboxylate metabolism, Biosynthesis of alkaloids derived from shikimate pathway, and Flavone and flavonol biosynthesis. This study lays a foundation for the later detection of differential metabolites and metabolic pathways for targeting, and provides a theoretical basis for disease-resistant breeding and the control of B. pervariabilis ¡Á D. grandis blight.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H68N | ChemSpider

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Aceclidine effects on outflow facility after ciliary muscle disinsertion

Aceclidine increases outflow facility with little accomodative effect. To determine whether this dissociation resides in the ciliary muscle (CM) or trabecular meshwork (TM), we measured aceclidine effects on perfusion outflow facility in both eyes of 8 rhesus monkeys after unilateral disinsertion of the CM from the TM. Facility in the control eyes increased by ~250% following intravenous pilocarpine and by an additional ~250% following intravenous pilocarpine and by an additional ~250% following intracameral pilocarpine, relative to baseline and uncorrected for washout. In CM-disinserted eyes, the facility response to intravenous and intracameral pilocarpine averaged ~25% of that in contralateral controls. Cytochalasin B, which acts directly on the TM to increase facility but is not additive to maximal pilocarpine doses in normal eyes, had no additional effect beyond that of pilocarpine in control eyes but induced an additional 100% facility increase relative to baseline in CM-disinserted eyes. The accomodative response to carbachol in CM-disinserted eyes was ~80% of that in contralateral controls, consistent with retention of CM contractility and the gonioscopic appearance of shallow CM disinsertion. Intracameral aceclidine HCl doses of 5 and 50 mug increased outflow facility by ~80 and 250%, respectively, in control eyes, and by ~0 and 80% in Cm-disinserted eyes. Either the low aceclidine dose affected facility via the CM, while the high dose exerted an additional effect on the TM, or aceclidine acted only via the CM, with the low dose being ineffective and the high dose modestly effective in CM-disinserted eyes because only a few CM-TM attachments remained.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H64N | ChemSpider

Reference 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

Aceclidine and pilocarpine interact differently with muscarinic receptor in isolated rabbit iris muscle

The relationship between muscarinic receptor affinity states and the contractile response to the muscarinic agonists carbachol, aceclidine, and pilocarpine, has been examined in the isolated rabbit iris muscle. Contraction of the iris muscle by carbachol and aceclidine was more potent and/or more efficacious than the response to pilocarpine. Analysis of [3H]- Quinuclidinyl benzilate (QNB) binding showed that while both carbachol and aceclidine bound to high- and low-affinity forms of the muscarinic receptor, pilocarpine bound to one affinity state. The efficacy of carbachol and aceclidine to stimulate contraction of the iris muscle was consistent with receptor occupancy theory only when considering the low-affinity state of the muscarinic receptor, and activation of the low-affinity rather than high-affinity binding state of the receptor is likely to mediate the contraction of iris muscle. Therefore, the typical anti-glaucoma muscarinic agonists aceclidine and pilocarpine may interact differently with their target receptors in isolated rabbit iris muscle.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H91N | ChemSpider

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M1 receptor agonist activity is not a requirement for muscarinic antinociception.

The analgesic effects of a series of muscarinic agonists were investigated by use of the mouse acetic acid writhing, grid-shock, hot-plate and tail-flick tests. The compounds tested were oxotremorine, pilocarpine, arecoline, aceclidine, RS86 and four 3-3(substituted-1,2,5-thiadiazol-4-yl)-1,2,5,6-tetrahy-dro-1 -methyl pyridines (substituted TZTP), these being propoxy-TZTP, 3-Cl-propylthio-TZTP, xanomeline (hexyloxy-TZTP) and hexylthio-TZTP. These agonists were also assayed for their ability to displace [3H]oxotremorine-M and [3H]pirenz-epine binding and for their functional selectivity at pharmaco-logic M1, M2 and M3 receptors. These compounds all produced dose-dependent antinociceptive effects in all of the mouse analgesia tests. The effects of oxotremorine in the writhing test were fully antagonized by the muscarinic antagonist scopolamine (0.1 mg/kg), but only partially antagonized by methsco-polamine (10 mg/kg) and unaffected by the opioid antagonist naltrexone. 3-Cl-propylthio-TZTP and propoxy-TZTP had virtually no effect at the M1 receptor subtype as measured by the human m1 clone expressed in baby hamster kidney cells or the rabbit vas deferens assay. These compounds, however, were more potent in the analgesia tests than the selective M1 agonists xanomeline and hexylthio-TZTP. These data suggest that muscarinic analgesia is mediated by central muscarinic receptors. However, activity at the M1 receptor subtype is not a requirement for antinociceptive activity.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H84N | ChemSpider

Electric Literature 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.

ACECLIDINE ISOMERS AND SCALEMIC MIXTURES THEREOF FOR THE TREATMENT OF PRESBYOPIA

The invention provides compositions containing aceclidine isomers and scalemic mixtures thereof for the treatment of presbyopia. The compositions optionally contain an alpha-adrenergic agonist, a cycloplegic agent, a cryoprotectant, a non-ionic surfactant and/or a viscosity enhancer.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H38N | ChemSpider

Synthetic Route 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.

COMPOSITIONS AND METHODS FOR THE TREATMENT OF PRESBYOPIA

The invention provides compositions and methods for the treatment of presbyopia. The compositions preferably comprise aceclidine, oxymetazoline, a cryoprotectant and a non-ionic surfactant. The compositions optionally contain a viscosity enhancer.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H37N | ChemSpider

Synthetic Route 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.

Synthesis of (R) and (S)-3-aminoquinuclidine from 3-quinuclidinone and (S) and (R)-1-phenethylamine

The synthesis of (R) and (S)-3-amino quinuclidine, an important building block for the synthesis of chiral 5-HT3 serotonin receptor antagonists, is described. The key reaction is the reduction by NaBH4 of the imine prepared from the 3-quinuclidinone and chiral (S) or (R)-1-phenethylamine.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H67N | ChemSpider

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

Quantitative Evaluation of the Reactivity of Alkylating Agents

A sensitive and reproducible method for quantitative evaluation of the relative reactivities of alkylating agents was developed, based on competitive alkylation.The method is superior to the known calorimetric methods.The reactivities of the agents could also be correlated with the 13C chemical shifts of the alpha-methylene.The method was successfully applied for the ranking of “soft” alkylating agents of low reactivity. – Keywords: Alkylating Agents, Soft Drugs, NMR Spectra, Competitive Alkylation, Soft Quaternary Salts

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Quinuclidine – Wikipedia,
Quinuclidine | C7H47N | ChemSpider