Brief introduction of 123536-14-1

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Chemistry is the science of change. But why do chemical reactions take place? Why do chemicals react with each other? The answer is in thermodynamics and kinetics.In a document type is Patent, the author is and a compound is mentioned, 123536-14-1, (R)-3-Aminoquinuclidine dihydrochloride, introducing its new discovery. name: (R)-3-Aminoquinuclidine dihydrochloride

Synthesis of combinatorial libraries of compounds reminiscent of natural products

The present invention provides complex compounds reminiscent of natural products and libraries thereof, as well as methods for their production. The inventive compounds and libraries of compounds are reminiscent of natural products in that they contain one or more stereocenters, and a high density and diversity of functionality. In general, the inventive libraries are synthesized from diversifiable scaffold structures, which are synthesized from readily available or easily synthesizable template structures. In certain embodiments, the inventive compounds and libraries are generated from diversifiable scaffolds synthesized from a shikimic acid based epoxyol template. In other embodiments, the inventive compounds and libraries are generated from diversifiable scaffolds synthesized from the pyridine-based template isonicotinamide. The present invention also provides a novel ortho-nitrobenzyl photolinker and a method for its synthesis. Furthermore, the present invention provides methods and kits for determining one or more biological activities of members of the inventive libraries. Additionally, the present invention provides pharmaceutical compositions containing one or more library members.

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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H131N | ChemSpider

Awesome Chemistry Experiments For (R)-3-Aminoquinuclidine dihydrochloride

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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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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H147N | ChemSpider

Simple exploration of (R)-3-Aminoquinuclidine dihydrochloride

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Design, synthesis, structure-activity relationship, and in vivo activity of azabicyclic aryl amides as alpha7 nicotinic acetylcholine receptor agonists

A novel set of azabicyclic aryl amides have been identified as potent and selective agonists of the alpha7 nAChR. A two-pronged approach was taken to improve the potential hERG liability of previously disclosed alpha7 nAChR agonist, PNU-282,987, while maintaining the compound’s other desirable pharmacological properties. The first approach involved further exploration of the aryl carboxylic acid fragment of PNU-282,987, while the second approach focused on modification of the azabicyclic amine portion of PNU-282,987. The best compounds from each series are characterized by rapid brain penetration, good oral bioavailability in rat, and demonstrate in vivo efficacy in a rat P50 auditory sensory gating assay. At least one analog from each series (1h, 1o, 2a, 9a, and 18a) shows an improved hERG safety profile over PNU-282,987.

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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H156N | ChemSpider

Awesome Chemistry Experiments For (R)-3-Aminoquinuclidine dihydrochloride

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QUINUCLIDINES SUBSTITUTED BENTODIOXINE CARBOXAMIDES FOR THE TREATMENT OF NEURODEGENERATIVE DISEASES

The invention provides the malate salt of compounds of Formula I, wherein X is malate salt, including D- or L-; wherein A is (a), wherein B is (b) or pharmaceutical composition, racemic mixture, or pure enantiomer thereof. The compounds of Formula I are useful to treat diseases or conditions in which alpha7 is known to be involved.

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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H130N | ChemSpider

New explortion of 827-61-2

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METHODS FOR TREATING MUSCULAR DYSTROPHIES

Provided herein are methods for treating and preventing a disease related to diminution or dysfunction of a dystrophin-related complex in a subject in need thereof, comprising administering to the subject a compound that increases sarcospan. Also provided herein are pharmaceutical compositions comprising a compound that increases sarcospan, or a pharmaceutically acceptable salt or ester thereof, useful for the treatments described herein.

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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H32N | ChemSpider

Properties and Exciting Facts About Quinuclidin-4-ylmethanamine

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2 – Substituted cephem compound-containing pharmaceutical composition (by machine translation)

PROBLEM TO BE SOLVED: To provide a cephem compound which has a strong antimicrobial activity, in particular effective against various beta-lactamase producing Gram negative bacteria, and a composition comprising the compound.SOLUTION: The present invention provides a pharmaceutical composition comprising a compound represented by formula (I), an ester at a carboxyl group, an amino-protected compound when the amino is present on a ring in the 7-side chain, or a pharmaceutically acceptable salt thereof.

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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H26N | ChemSpider

Awesome Chemistry Experiments For APR-246

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The benefit of reactivating p53 under MAPK inhibition on the efficacy of radiotherapy in melanoma

Radiotherapy (RT) in patients with melanoma historically showed suboptimal results, because the disease is often radioresistant due to various mechanisms such as scavenging free radicals by thiols, pigmentary machinery, or enhanced DNA repair. However, radiotherapy has been utilized as adjuvant therapy after the complete excision of primary melanoma and lymph nodes to reduce the rate of nodal recurrences in high-risk patients. The resistance of melanoma cells to radiotherapy may also be in relation with the constitutive activation of the MAPK pathway and/or with the inactivation of p53 observed in about 90% of melanomas. In this study, we aimed to assess the potential benefit of adding RT to BRAF-mutated melanoma cells under a combined p53 reactivation and MAPK inhibition in vitro and in a preclinical animal model. We found that the combination of BRAF inhibition (vemurafenib, which completely shuts down the MAPK pathway), together with p53 reactivation (PRIMA-1Met) significantly enhanced the radiosensitivity of BRAF-mutant melanoma cells. This was accompanied by an increase in both p53 expression and activity. Of note, we found that radiation alone markedly promoted both ERK and AKT phosphorylation, thus contributing to radioresistance. The combination of vemurafenib and PRIMA-1Met caused the inactivation of both MAPK kinase and PI3K/AKT pathways. Furthermore, when combined with radiotherapy, it was able to significantly enhance melanoma cell radiosensitivity. Interestingly, in nude mice bearing melanoma xenografts, the latter triple combination had not only a synergistic effect on tumor growth inhibition, but also a potent control on tumor regrowth in all animals after finishing the triple combination therapy. RT alone had only a weak effect. In conclusion, we provide a basis for a strategy that may overcome the radioresistance of BRAF-mutated melanoma cells to radiotherapy. Whether this will translate into a rational to use radiotherapy in the curative setting in BRAF-mutated melanoma patients deserves consideration.

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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H171N | ChemSpider

Simple exploration of (R)-3-Aminoquinuclidine dihydrochloride

We¡¯ll also look at important developments in the pharmaceutical industry because understanding organic chemistry is important in understanding health, medicine, the role of 123536-14-1, and how the biochemistry of the body works.COA of Formula: C7H16Cl2N2

Chemistry is traditionally divided into organic and inorganic chemistry. COA of Formula: C7H16Cl2N2, The former is the study of compounds containing at least one carbon-hydrogen bonds.In a patent£¬Which mentioned a new discovery about 123536-14-1

ALKALOID ESTER AND CARBAMATE DERIVATIVES AND MEDICINAL COMPOSITIONS THEREOF

Compounds according to formula (I) are effective for the treatment of broncho-obstructive and inflammatory diseases.

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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H92N | ChemSpider

Extracurricular laboratory:new discovery of (R)-3-Aminoquinuclidine dihydrochloride

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1,4-DISUBSTITUTED 1,2,3-TRIAZOLES, METHODS FOR PREPARING SAME, AND DIAGNOSTIC AND THERAPEUTIC USES THEREOF

A compound having the following general formula (I): wherein: X is a nitrogen atom and Y is a carbon atom; or X is a carbon atom and Y is a nitrogen atom; the Ar group is an aryl or heteroaryl group; and the RN and RN? groups, together with the carbon atoms to which they are bound, form a monocyclic or bicyclic azacycloalkane group. The pharmaceutically acceptable salts thereof, the hydrates or polymorphic crystalline structures thereof, and to the racemates, diastereoisomers, or enantiomers thereof are also described.

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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H127N | ChemSpider

Extracurricular laboratory:new discovery of 827-61-2

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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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Reference£º
Quinuclidine – Wikipedia,
Quinuclidine | C7H71N | ChemSpider