Some scientific research about (R)-3-Aminoquinuclidine dihydrochloride

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Synthesis, crystal structures, second harmonic generation response and temperature phase transitions of two noncentrosymmetric Cu(II)-hybrid halides compounds: [(R)-C7H16N2][CuX4] (X = Cl or Br)

(R)-(+)-3-aminoquinuclidine was used in the synthesis of [(R)-C7H16N2][CuCl4] (1) and [(R)-C7H16N2][CuBr4] (2), which both contain similar [CuX4]2- anions (X = Cl or Br). The structures of the two compounds were determined using single-crystal X-ray diffraction. The use of enantiomerically pure sources of (R)-C7H14N2 forces crystallographic noncentrosymmetry. These materials crystallize in the chiral space group P212121 (No. 19), which exhibits the enantiomorphic crystal class 222 (D2). In the molecular arrangement, the [CuX4]2- anions are linked to the organic cations through N?H ? X and C?H ? X hydrogen bonds to form cation-anion-cation molecular units, which are held together by means of offset face-to-face interactions giving a three-dimensional network. Thermal stability of the crystals was ascertained by TG measurement. Compounds (1) and (2) display several phases transition with higher transition temperature at T = 100 C. The Kurtz and Perry powder method using Nd:YAG laser shows that their second harmonic generation (SHG) efficiencies are about 0.81 and 0.82 times as large as that of KH2PO4 (KDP), respectively. Such a chiral hybrid metal halides skeleton could provide a new platform for future engineering in the areas including information storage, light modulators and optoelectronic functionalities.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H145N | ChemSpider

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Correlation between pKa and reactivity of quinuclidine-based catalysts in the Baylis-Hillman reaction: Discovery of quinuclidine as optimum catalyst leading to substantial enhancement of scope

The reactivity of a variety of quinuclidine-based catalysts in the Baylis-Hillman reaction has been examined, and a straightforward correlation between the basicity of the base and reactivity has been established, without exception. The following order of reactivity was established with pKa’s of the conjugate acids (measured in water) given in parentheses: quinuclidine (11.3), 3-hydroxyquinuclidine (9.9), DABCO (8.7), 3-acetoxyquinuclidine (9.3), 3-chloroquinuclidine (8.9), and quinuclidinone (7.2). The higher than expected reactivity of DABCO, based on its pKa, was analyzed by comparing the relative basicity of DABCO and 3-acetoxyquinuclidine in DMSO. It was found that in aprotic solvent, DABCO was 0.6 pKa units more basic than 3-acetoxyquinuclidine, thus establishing a direct link between pKa of the amine and its reactivity. In contrast to previous literature work that reported the contrary, quinuclidine, which has the highest pKa, was found to be the most active catalyst. The reaction profile with quinuclidine showed significant autocatalysis, which suggested that the presence of proton donors might further enhance rates. Thus, a series of additives bearing polar X-H bonds were investigated and it was found that methanol, triethanolamine, formamide, and water all provided additional acceleration. Methanol was found to be optimum, and the powerful combination of quinuclidine with methanol was tested with a host of aldehydes and Michael acceptors. Not only were the reactions more efficient and faster than previously reported, but now new substrates that were previously unreactive could be employed. Notable examples include the use of acetylenic aldehydes and the employment of vinyl sulfones, acrylamides, delta-lactones, and even alpha,beta-unsaturated esters bearing a beta-substituent.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H45N | ChemSpider

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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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PRIMA-1Met/APR-246 displays high antitumor activity in multiple myeloma by induction of p73 and noxa

Targeting p53 by the small-molecule PRIMA-1Met/APR-246 has shown promising preclinical activity in various cancer types.However, the mechanism of PRIMA-1Met-induced apoptosis is not completely understood and its effect on multiple myeloma cells is unknown. In this study, we evaluated antitumor effect of PRIMA-1Met alone or its combination with current antimyeloma agents in multiple myeloma cell lines, patient samples, and a mouse xenograft model. Results of our study showed that PRIMA-1Met decreased the viability of multiple myeloma cells irrespective of p53 status, with limited cytotoxicity toward normal hematopoietic cells. Treatment of multiple myeloma cells with PRIMA-1Met resulted in induction of apoptosis, inhibition of colony formation, and migration. PRIMA-1Met restored wild-type conformation of mutant p53 and induced activation of p73 upregulating Noxa and downregulating Mcl-1 without significant modulation of p53 level. siRNAmediated silencing of p53 showed a little effect on apoptotic response of PRIMA-1Met, whereas knockdown of p73 led to substantial attenuation of apoptotic activity in multiple myeloma cells, indicating that PRIMA-1Met- induced apoptosis is, at least in part, p73-dependent.Importantly, PRIMA-1Met delayed tumor growth and prolonged survival of mice bearing multiple myeloma tumor. Furthermore, combined treatment of PRIMA-1Met with dexamethasone or doxorubicin displayed synergistic effects in both multiple myeloma cell lines and primary multiple myeloma samples. Consistent with our in vitro observations, cotreatment with PRIMA-1Met and dexamethasone resulted in enhanced antitumor activity in vivo. Our study for the first time shows antimyeloma activity of PRIMA-1Met and provides the rationale for its clinical evaluation in patients with multiple myeloma, including the high-risk group with p53 mutation/deletion. Mol Cancer Ther; 12(11); 2331-41.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H174N | ChemSpider

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In heterogeneous catalysis, the catalyst is in a different phase from the reactants. COA of Formula: C7H16Cl2N2, At least one of the reactants interacts with the solid surface in a physical process called adsorption in such a way. 123536-14-1, name is (R)-3-Aminoquinuclidine dihydrochloride. In an article£¬Which mentioned a new discovery about 123536-14-1

Azabicyclic carbamates and their use as alpha-7 nicotinic acetylcholine receptor agonists

The invention provides compounds of formula (I) wherein n, A, R1, R2 and R3 are as defined in the description, and the preparation thereof. The compounds of formula (I) are useful as pharmaceuticals.

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Quinuclidine – Wikipedia,
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Comparison of the muscarinic receptor binding activity of some tertiary amines and their quaternary ammonium analogues

A series of tertiary amines and their N-methyl quaternary salts were examined for their ability to inhibit specific [3H]3-quinuclidinyl benzilate binding to rat brain muscarinic receptors. The more flexible tertiary amines, like dimethylaminoethyl acetate, were less potent than their respective quaternary ammonium analogues, while rigid tertiary amines, like aceclidine, were more potent than their quaternary derivatives. The competition curves of most of the compounds were adequately described by a two-site binding equation. A good correlation between pharmacological activity and the high-affinity dissociation constant was observed. The influence of pH in the competitive inhibition of [3H]3-quinuclidinyl benzilate binding by arecoline and scopolamine was also examined. The potency of these amines declined relative to that of their N-methyl derivatives as the pH increased from 8.90 to 9.0, suggesting that it is primarily the protonated form of arecoline and scopolamine which interacts with the muscarinic receptor.

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5291-32-7, Name is APR-246, belongs to quinuclidine compound, is a common compound. name: APR-246In an article, once mentioned the new application about 5291-32-7.

USE OF ERIBULIN AND 3-QUINUCLIDINONE DERIVATIVES IN THE TREATMENT OF CANCER

The invention features methods for treating and preventing cancer (e.g., a p53-mutated cancer) in a patient in need thereof by administering eribulin (e.g., eribulin mesylate) in combination with a 3-quinuclidinone derivative (e.g., PRIMA-1 or PRIMA-1MET).

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NEW STRATEGIES FOR TREATING MELANOMA

The present invention relates to a p53-activating agent capable of transferring wild-type tumor protein p53 (p53) from an inactive conformation into an active conformation capable of inducing apoptosis, for use in the treatment of melanoma, wherein said p53-activating agent is administered simultaneously or sequentially with a BRAF-inhibiting agent capable of inhibiting activity of serine/threonine-protein kinase B-Raf (BRAF) comprising an activating mutation.

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Quinuclidine – Wikipedia,
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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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Process for preparing quinuclidine enantiomers

A new composition of matter, (+) 3-acetoxy- quinuclidine and its salts, ophthalmic compositions comprising this compound or any of its physiologically acceptable salts in a suitable carrier such as a phosphate buffer, and a process of preparation of the active ingredients, which comprises esterifying quinuclidinol so as to obtain racemic 3-lower-alkoxy quinuclidine, subjecting same to enzymatic hydrolysis by a cholinesterase so as to selectively hydrolyze the (-) isomer, separating the unchanged (+) lower-alkoxy quinuclidine, hydrolyzing the latter and esterifying it to the desired compound. Amongst various homolophes the preferred compound is (+)3-acetoxy quinuclidine as this is pharmaceutically the most potent one.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H43N | ChemSpider