Tag: M.W=200-300

This type of reactivity has quickly become one of the cornerstones of modern catalysis. The transformation of simple hydrocarbons into more complex products via catalytic C–H bond functionalisation has revolutionised modern synthetic chemistry. 6753-98-6, Name is (1E,4E,8E)-2,6,6,9-Tetramethylcycloundeca-1,4,8-triene. In a pantent, once mentioned the new application about 6753-98-6, Recommanded Product: 6753-98-6.

Experimental model of escape phenomenon in hamsters and the effectiveness of YM-53601 in the model

1 The aim of this study was to establish an experimental model of the escape phenomenon, in which plasma cholesterol, initially reduced by a 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase inhibitor such as pravastatin, increases again on long-term administration. We also evaluated the efficacy of YM-53601 ((E)-2-[2-fluoro-2- (quinuclidin-3-ylidene) ethoxy]-9H-carbazole monohydrochloride), a squalene synthase inhibitor, in this model. 2 Pravastatin inhibited cholesterol biosynthesis in hamster primary hepatocytes (IC50, 14 nM). After pre-treatment with pravastatin, in contrast, almost no effect on cholesterol biosynthesis was seen. 3 In hamsters fed a high fat diet, 3 mg kg(-1) pravastatin for 9 days decreased plasma non-HDL cholesterol (total cholesterol-high density lipoprotein cholesterol) (P<0.01), but this effect was lost between 17 and 27 days of treatment, accompanied by an increase in HMG-CoA reductase activity. No such increase in plasma non-HDL cholesterol was seen with YM-53601 at 30 mg kg(-1) after 9 (P<0.001), 17 (P<0.01) or 27 (P<0.001) days of treatment. Replacement of pravastatin with YM-53601 caused a decrease in plasma non-HDL cholesterol by 53% (P<0.001) and in HMG-CoA reductase activity. 4 This animal model thus satisfactorily replicates the escape phenomenon observed in humans and may therefore be useful in evaluation of lipid-lowering agents, specifically comparison of HMG-CoA reductase inhibitors. Further, YM-53601 may be useful in the treatment of hypercholesterolemia without induction of the escape phenomenon. Note that a catalyst decreases the activation energy for both the forward and the reverse reactions and hence accelerates both the forward and the reverse reactions.If you’re interested in learning more about 6753-98-6. The above is the message from the blog manager. Recommanded Product: 6753-98-6.

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Quinuclidine – Wikipedia,
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Redox catalysis has been broadly utilized in electrochemical synthesis due to its kinetic advantages over direct electrolysis. The appropriate choice of redox mediator can avoid electrode passivation and overpotential. 68131-04-4, Name is Sodium bicyclo[2.2.1]hept-5-ene-2,3-dicarboxylate, SMILES is O=C([O-])C1C(C([O-])=O)C2C=CC1C2.[Na+].[Na+], in an article , author is NORDVALL, G, once mentioned of 68131-04-4, Safety of Sodium bicyclo[2.2.1]hept-5-ene-2,3-dicarboxylate.

3-LITHIOQUINUCLIDIN-2-ENE – A NOVEL INTERMEDIATE FOR THE SYNTHESIS OF MUSCARINIC AGONISTS AND ANTAGONISTS

A method for the generation of 3-lithioquinuclidin-2-ene (3) as a nucleophilic intermediate for the synthesis of 3-substituted quinuclidin-2-enes is presented.

Consequently, the presence of a catalyst will permit a system to reach equilibrium more quickly, but it has no effect on the position of the equilibrium as reflected in the value of its equilibrium constant.Interested yet? Keep reading other articles of 68131-04-4, you can contact me at any time and look forward to more communication. Safety of Sodium bicyclo[2.2.1]hept-5-ene-2,3-dicarboxylate.

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Quinuclidine – Wikipedia,
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Chemo-enzymatic cascade processes are invaluable due to their ability to rapidly construct high-value products from available feedstock chemicals in a one-pot relay manner.In an article, author is Kobayashi, S, once mentioned the application of 13419-61-9, Name is Sodium decane-1-sulfonate, molecular formula is C10H21NaO3S, molecular weight is 244.3267, MDL number is MFCD00007526, category is quinuclidine. Now introduce a scientific discovery about this category, Category: quinuclidines.

Effects of YM905, a novel muscarinic M-3-receptor antagonist, on experimental models of bowel dysfunction in vivo

We investigated the effects of YM905 [(+)-(1S,3’R)-quinuclidin-3′-yl 1-phenyl-1,2,3,4-tetrahydroisoquinoline-2-carboxylate monosuccinate], a new orally active muscarinic M-3-receptor antagonist, on bowel dysfunction in vivo using experimental models that reproduce the symptoms present in irritable bowel syndrome (IBS). YM905 potently inhibited restraint stress-induced fecal pellet output in fed rats (ED50: 4.0 mg/kg) and diarrhea in fasted rats (ED50: 1.7 mg/kg), with similar potencies to the inhibition of bethanechol-, neostigmine- and nicotine-induced fecal pellet output in rats (ED50: 3.3, 7.9 and 4.5 mg/kg, respectively). YM905 also inhibited 5-hydroxytryptamine (5-HT)-, prostaglandin E-2- and castor oil-induced secretory diarrhea in mice (ED50: 5.5, 14 and 6.3 mg/kg, respectively), but showed no significant effect on cholera toxin-induced intestinal secretion in mice. In addition, YM905 (3, 10 mg/kg) reversed morphine-decreased postprandial defecation in ferrets, a model of spastic constipation, whereas remosetron, a 5-HT3-receptor antagonist, was not effective. The mode of YM905 action was similar to that of darifenacin, a selective M3-receptor antagonist, with equivalent potencies. By contrast, propantheline, an antimuscarinic drug that has been used for IBS, was much less potent. These results show that YM905 ameliorates a wide spectrum of bowel dysfunctions through the blockade Of M-3 receptors, suggesting its therapeutic potential for treating IBS.

The reactant in an enzyme-catalyzed reaction is called a substrate. Enzyme inhibitors cause a decrease in the reaction rate of an enzyme-catalyzed reaction.Interested yet? Keep reading other articles of 13419-61-9, you can contact me at any time and look forward to more communication. Category: quinuclidines.

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Chemistry is a science major with cience and engineering. The main research directions are chemical synthesis,preparation and modification of special coatings, and research on the structure and performance of functional materials. 51997-51-4, Name is 4-Glycidyloxycarbazole, SMILES is C1(NC2=C3C=CC=C2)=C3C(OCC4CO4)=CC=C1, belongs to quinuclidine compound. In a document, author is Madadi, Nikhil Reddy, introduce the new discover, Product Details of 51997-51-4.

Evaluation of (Z)-2-((1-benzyl-1H-indol-3-yl)methylene)-quinuclidin-3-one analogues as novel, high affinity ligands for CB1 and CB2 cannabinoid receptors

A small library of N-benzyl indolequinuclidinone (IQD) analogs has been identified as a novel class of cannabinoid ligands. The affinity and selectivity of these IQDs for the two established cannabinoid receptor subtypes, CB1 and CB2, was evaluated. Compounds 8 (R = R-2 = H, R-1 = F) and 13 (R = COOCH3, R-1 = R-2 = H) exhibited high affinity for CB2 receptors with K-i values of 1.33 and 2.50 nM, respectively, and had lower affinities for the CBI receptor (K-i values of 9.23 and 85.7 nM, respectively). Compound 13 had the highest selectivity of all the compounds examined, and represents a potent cannabinoid ligand with 34-times greater selectivity for CB2R over CB1R. These findings are significant for future drug development, given recent reports demonstrating beneficial use of cannabinoid ligands in a wide variety of human disease states including drug abuse, depression, schizophrenia, inflammation, chronic pain, obesity, osteoporosis and cancer. (C) 2013 Elsevier Ltd. All rights reserved.

Each elementary reaction can be described in terms of its molecularity, the number of molecules that collide in that step. The slowest step in a reaction mechanism is the rate-determining step.Interested yet? Keep reading other articles of 51997-51-4, you can contact me at any time and look forward to more communication. Product Details of 51997-51-4.

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Quinuclidine – Wikipedia,
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Reactions catalyzed within inorganic and organic materials and at electrochemical interfaces commonly occur at high coverage and in condensed media, causing turnover rates to depend strongly on interfacial structure and composition, Like 31906-04-4, Name is 4-(4-Hydroxy-4-methylpentyl)cyclohex-3-enecarbaldehyde. In a document, author is Dolle, F, introducing its new discovery. Recommanded Product: 4-(4-Hydroxy-4-methylpentyl)cyclohex-3-enecarbaldehyde.

Highly efficient synthesis of [C-11]Me-QNB, a selective radioligand for the quantification of the cardiac muscarinic receptors using PET

Me-QNB (N-methyl-quinuclidin-3-yl benzilate or N-methyl-quinuclidin-3-yl diphenylhydroxy acetate) is a hydrophilic, non-metabolized and highly specific muscarinic acetylcholinergic antagonist. Using this quaternary ammonium derivative of QNB, labelled with carbon-11, a positron-emitting isotope (half-life : 20.4 minutes), the potential for quantification of myocardial muscarinic receptors in vivo using the high-resolution, sensitive and quantitative imaging technique PET (positron emission tomography) was previously demonstrated in dogs and validated in humans. In this paper, the radiosynthesis of carbon-11-labelled Me-QNB is investigated and oriented towards the preparation of multi milliCuries of radiotracer. Typically, using no-carrier-added [C-11]methyl triflate as the alkylating agent and 0.64 mg (1.89 mu mol) of QNB as precursor for labelling at 100 degreesC for 1 minute lead to a 48.5% +/- 10% (15 runs) decay-corrected radiochemical yield (based on [C-11]methyl triflate). 183 mCi (+/- 39) of [C-11]Me-QNB ([C-11]-1) could be synthesized in only 27 to 28 minutes after EOB and occasionally, up to 340 mCi of [C-11]Me-QNB ([C-11]-1) were obtained, corresponding to a 85% decay-corrected yield. The associated decay-corrected specific radioactivities obtained were 2658 mCi/mu mol (+/- 971) at EOB.

One of the oldest and most widely used commercial enzyme inhibitors is aspirin, which selectively inhibits one of the enzymes involved in the synthesis of molecules that trigger inflammation. 31906-04-4, you can contact me at any time and look forward to more communication. Recommanded Product: 4-(4-Hydroxy-4-methylpentyl)cyclohex-3-enecarbaldehyde.

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Quinuclidine – Wikipedia,
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Enzyme inhibitors cause a decrease in the reaction rate of an enzyme-catalyzed reaction by binding to a specific portion of an enzyme and thus slowing or preventing a reaction from occurring. 2425-77-6, Name is 2-Hexyl-1-decanol, molecular formula is C16H34O, belongs to quinuclidine compound, is a common compound. In a patnet, author is Tang, Cuyue, once mentioned the new application about 2425-77-6, Formula: C16H34O.

Neuropharmacokinetics of two investigational compounds in rats: Divergent temporal profiles in the brain and cerebrospinal fluid

Two investigational compounds (FRM-1, (R)-7-fluoro-N-(quinuclidin-3-yl)benzo[b]thiophene-2-carboxamide and FRM-2, (R)-7-cyano-N-(quinuclidin-3-yl)benzo[b]thiophene-2-carboxamide) resided in rat brain longer than in systemic circulation. In Caco-2 directional transport studies, they both showed good intrinsic passive permeability but differed significantly in efflux susceptibility (efflux ratio of <2 and similar to 7, respectively), largely attributed to P-glycoprotein (P-gp). Capitalizing on these interesting properties, we investigated how cerebrospinal fluid (CSF) concentration (C-CSF) would be shaped by unbound plasma concentration (C-u,C-p) and unbound brain concentration (C-u,C-b) in disequilibrium conditions and at steady state. Following subcutaneous administration, FRM-1 C-CSF largely followed C-u,C-p initially and leveled between C-u,C-p and C-u,C-b. However, it gradually approached C-u,C-b and became lower than, but parallel to C-u,C-b at the terminal phase. In contrast, FRM-2 C-CSF temporal profile mostly paralleled the C-u,C-p but was at a much lower level. Upon intravenous infusion to steady state, FRM-1 C-CSF and C-u,C-b were similar, accounting for 61% and 69% of the Cu, indicating a case of largely passive diffusion-governed brain penetration where C-CSF served as a good surrogate for C-u,C-b. On the contrary, FRM-2 C-CSF and C-u,C-b were remarkably lower than C-u,C-p, (17% and 8% of C-u,C-p respectively), suggesting that FRM-2 brain penetration was severely impaired by P-gp-mediated efflux and C-CSF underestimated this impact. A semi-physiologically based pharmacokinetic (PBPK) model was constructed that adequately described the temporal profiles of the compounds in the plasma, brain and CSF. Our work provided some insight into the relative importance of blood-brain barrier (BBB) and blood-CSF barrier (BCSFB) in modulating CCSF. (C) 2014 Elsevier Inc. All rights reserved. The reactant in an enzyme-catalyzed reaction is called a substrate. Enzyme inhibitors cause a decrease in the reaction rate of an enzyme-catalyzed reaction.Interested yet? Keep reading other articles of 2425-77-6, you can contact me at any time and look forward to more communication. Formula: C16H34O.

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Quinuclidine – Wikipedia,
,Quinuclidine | C7H13N | ChemSpider

Chemo-enzymatic cascade processes are invaluable due to their ability to rapidly construct high-value products from available feedstock chemicals in a one-pot relay manner.In an article, author is Primozic, Ines, once mentioned the application of 6846-50-0, Name is 2,2,4-Trimethylpentane-1,3-diyl bis(2-methylpropanoate), molecular formula is C16H30O4, molecular weight is 286.41, MDL number is MFCD00059267, category is quinuclidine. Now introduce a scientific discovery about this category, Quality Control of 2,2,4-Trimethylpentane-1,3-diyl bis(2-methylpropanoate).

Influence of the Acyl Moiety on the Hydrolysis of Quinuclidinium Esters Catalyzed by Butyrylcholinesterase

Eight chiral esters of quinuclidin-3-ol and butyric, acetic, pivalic and benzoic acid were synthesized as well as their racemic and chiral, quaternary N-benzyl derivatives. All racemic and chiral quaternary compounds were studied as substrates and/or inhibitors of horse serum butyrylcholinesterase (BChE). The best substrate for the enzyme was (R)-N-benzyl butyrate. The rates of hydrolysis decreased in order (R)-butyrate >> (R)-acetate (7-fold slower) > (R)-pivalate (8-fold slower) > (R)-benzoate (9-fold slower reaction), while (S)-N-benzyl esters were much poorer substrates (320 (butyrate) – 4360-fold slower (pivalate) than the appropriate (R)-enantiomer). For all (S)-N-benzyl esters excluding (S)-N-benzyl acetate inhibition constants were determined (K-a = 3.3-60 mu mol dm(-3)). The hydrolysis of racemic mixtures of N-benzyl esters proceeded 1.4 (for acetate) – 5.1 (for benzoate) times slower than that of pure (R)-enantiomers of the corresponding concentrations due to the inhibition with (S)-enantiomers. Change of the acyl moiety of the substrate effected both activity and stereoselectivity of the BChE.(doi: 10.5562/cca1829)

Enzymes are biological catalysts that produce large increases in reaction rates.Do you like my blog? If you like, you can also browse other articles about this kind. Thanks for taking the time to read the blog about 6846-50-0, Quality Control of 2,2,4-Trimethylpentane-1,3-diyl bis(2-methylpropanoate).

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Quinuclidine – Wikipedia,
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Chemistry is a science major with cience and engineering. The main research directions are chemical synthesis,preparation and modification of special coatings, and research on the structure and performance of functional materials. 13419-61-9, Name is Sodium decane-1-sulfonate, SMILES is CCCCCCCCCCS(=O)([O-])=O.[Na+], belongs to quinuclidine compound. In a document, author is Bruss, M, introduce the new discover, Formula: C10H21NaO3S.

Pharmacological differences and similarities between the native mouse 5-HT3 receptor in N1E-115 cells and a cloned short splice variant of the mouse 5-HT3 receptor expressed in HEK 293 cells

Human embryonic kidney (HEK) 293 cells were stably transfected with the cDNA encoding the short splice variant of the mouse 5-HT3 receptor (m5-HT3A(b); isolated by RT-PCR from NG108-15 cells) and its pharmacological properties were compared with those of the native 5-HT3 receptor of the mouse neuroblastoma cell line N1E-115. The m5-HT3A(b) receptor of N1E-115 cells differs from that isolated from NG108-15 cells by one amino acid (Val instead of lie) at position 52 of the amino acid sequence. Both radioligand binding studies with the selective 5-HT3 receptor antagonist [H-3]GR65630 (3-(5-methyl-1H-imidazol-4-yl)-1-(1-methyl-1H-indol-3-yl)-1-propanone) and functional experiments by measurement of [C-14]guanidinium influx evoked by 5-HT in the absence and presence of 10 mu M substance P were carried out. Binding of [H-3]GR65630 to the recombinant receptor in HEK 293 cells and the native receptor in N1E-115 cells was specific and of high affinity (K-d 4.4 and 3.0 nM, respectively) and characterized by B-max values of 875 and 1414 fmol/mg protein, respectively. At 10 nM [H-3]GR65630, specific binding was inhibited by the selective 5-HT3 receptor antagonist ondansetron (K-i II and 42 nM, respectively) and by 5-HT (K-i 294 and 563 nM, respectively). In the transfected HEK 293 cells, 5-HT induced an influx of [C-14]guanidinium both in the absence (pEC(50) 5.7) and presence of substance P (pEC(50) 6.6,) which was counteracted by 0.3 mu M ondansetron; in the N1E-115 cells, 5-HT also evoked [C-14]guanidinium influx in the absence (pEC(50) 6.0) and presence of substance P (pEC(50) 6.0). Both in transfected HEK 293 cells and in N1E-115 cells, the 5-HT receptor ligand RS-056812-198 ((R)-N-(quinuclidin-3-yl)-2-( l-methyl-l H-indol-3-yl)-2-oxo-acetamide; in the presence of substance P) induced an influx of [C-14]guanidinium (pEC(50) 9.8 and 8.7, respectively) with a maximum of about 70 and 30% of the maximum response to 5-HT, respectively. 5-HT tin the presence of substance P)-induced [C-14]guanidinium influx was inhibited by the imidazoline BDF 6143 (4-chloro-2(2-imidazolin-2-ylamino)-isoindoline; pIC(50) 4.9 and 5.3, respectively) and by the zeta-site ligand (+/-)-ifenprodil (pIC(50) 5.0 and 5.2, respectively). In conclusion, most of the drugs exhibited practically identical properties at both the recombinant m5-HT3A(b) receptor in HEK 293 cells and the native m5-HT3 receptor of N1E-115 cells. However, the recombinant receptor had a higher affinity for ondansetron, and the potency of 5-HT in inducing cation influx through the recombinant, but not through the native receptor, was increased by substance P. RS-056812-198 was a 10-fold more potent partial agonist at the recombinant than at the native receptor. These differences may be due to cell-specific post-translational modifications of the 5-HT3 receptor protein in the two cell lines, to the expression of other subunits in addition to the m5-HT3A(b) receptor in N1E-115 cells and/or to the difference in the amino acid sequence at position 52 of the short splice variants of the m5-HT3 receptors expressed in the two cell lines.

One of the oldest and most widely used commercial enzyme inhibitors is aspirin, which selectively inhibits one of the enzymes involved in the synthesis of molecules that trigger inflammation. 13419-61-9, you can contact me at any time and look forward to more communication. Formula: C10H21NaO3S.

Reference:
Quinuclidine – Wikipedia,
,Quinuclidine | C7H13N | ChemSpider

In classical electrochemical theory, both the electron transfer rate and the adsorption of reactants at the electrode control the electrochemical reaction. 253168-94-4, Name is 1-(3-Ethoxy-4-methoxyphenyl)-2-(methylsulfonyl)ethanamine, SMILES is O=S(CC(N)C1=CC=C(OC)C(OCC)=C1)(C)=O, in an article , author is Niphade, Navnath C., once mentioned of 253168-94-4, Formula: C12H19NO4S.

Efficient and single pot process for the preparation of enantiomerically pure solifenacin succinate, an antimuscarinic agent

The development of an efficient and economic one-pot process, in which the configuration of the chiral centers of the starting materials is retained, for the preparation of highly pure solifenacin succinate, an antimuscarinic agent, is presented in this communication. The earlier reported processes suffer from the drawbacks of racemization and low yields due to the use of strong base, higher temperatures, and longer reaction times. The present work circumvents these issues by activating (3R)-quinuclidin-3-ol into a mixed active carbonate derivative by treating it with bis(4-nitrophenyl)carbonate. The subsequent reaction of the active carbonate with an enantiomerically pure amine without using any base at ambient temperature provided enantiomerically pure solifenacin with an overall yield of 90%.

Note that a catalyst decreases the activation energy for both the forward and the reverse reactions and hence accelerates both the forward and the reverse reactions.If you’re interested in learning more about 253168-94-4. The above is the message from the blog manager. Formula: C12H19NO4S.

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Quinuclidine – Wikipedia,
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Chemistry is a science major with cience and engineering. The main research directions are chemical synthesis,preparation and modification of special coatings, and research on the structure and performance of functional materials. 957-68-6, Name is 7-Aminocephalosporanic acid, SMILES is CC(OCC(CS[C@@]([H])(N12)[C@H](N)C2=O)=C1C(O)=O)=O, belongs to quinuclidine compound. In a document, author is Prishchenko, A. A., introduce the new discover, Category: quinuclidines.

Addition of tris(trimethylsilyl) phosphite to quinuclidin-3-one and its carbocyclic analogs

Convenient methods of synthesis of functionalized phosphonic acids and their trimethylsilyl esters containing quinuclidine, adamantine, and bornane (camphane) moieties, involving reactions of tris(trimethylsilyl) phosphite with quinuclidin-3-one and its carbocyclic analogs.

Enzymes are biological catalysts that produce large increases in reaction rates.Do you like my blog? If you like, you can also browse other articles about this kind. Thanks for taking the time to read the blog about 957-68-6, Category: quinuclidines.

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Quinuclidine – Wikipedia,
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