Tag: M.W:100-200

Chemistry is traditionally divided into organic and inorganic chemistry. The former is the study of compounds containing at least one carbon-hydrogen bonds. 25952-53-8, Name is 1-(3-Dimethylaminopropyl)-3-ethylcarbodiimide hydrochloride, molecular formula is C8H18ClN3, belongs to quinuclidines compound, is a common compound. In a patnet, author is HACKSELL, U, once mentioned the new application about 25952-53-8, Recommanded Product: 1-(3-Dimethylaminopropyl)-3-ethylcarbodiimide hydrochloride.

QUINUCLIDIN-2-ENE – BASED MUSCARINIC ANTAGONISTS

A series of achiral 3-heteroaryl substituted quinuclidin-2-ene derivatives and related compounds have been synthesized by facile methods. The compounds were evaluated for muscarinic and antimuscarinic properties in receptor binding studies using (-)-[H-3]-QNB as the radioligand and ina functional assay using isolated guinea pig urinary bladder. 3-(2-Benzofuranyl)-quinuclidin-2-ene (15) displayed the highest M(1)-receptor affinity in the present series (K-i = 9.6 nM).

We¡¯ll also look at important developments in the pharmaceutical industry because understanding organic chemistry is important in understanding health, medicine, 25952-53-8. The above is the message from the blog manager. Recommanded Product: 1-(3-Dimethylaminopropyl)-3-ethylcarbodiimide hydrochloride.

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

Synthetic Route of 611-10-9, Children learn through play, and they learn more than adults might expect. Science experiments are a great way to spark their curiosity, 611-10-9, Name is Ethyl 2-oxocyclopentanecarboxylate, SMILES is C(OC(C1C(CCC1)=O)=O)C, belongs to quinuclidines compound. In a article, author is Brown, GR, introduce new discover of the category.

Novel optimised quinuclidine squalene synthase inhibitors

Optimised quinuclidine squalene synthase (SQS) inhibitors are reported; 3-[2-(2-allyl-4-(2-ethoxy carbonylethyl)phenyl)ethynyl]quinuclidin-3-ol 1c, is a potent inhibitor of rat (KI = 6 nM) and human (KI = 43 nM) microsomal SQS; the oral ED(50) of 1c, for the inhibition of rat cholesterol biosynthesis was 1.3+/-0.45 mg/kg and for the R-enantiomer 1m, 0.8+/-0.2 mg/kg, with the corresponding R-carboxylic acid 6a, being 0.9+/-0.25 mg/kg. (C) 1997 Elsevier Science Ltd. All rights reserved.

Synthetic Route of 611-10-9, Because enzymes can increase reaction rates by enormous factors and tend to be very specific, typically producing only a single product in quantitative yield, they are the focus of active research.you can also check out more blogs about 611-10-9.

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

One of the major reasons for studying chemical kinetics is to use measurements of the macroscopic properties of a system, such as the rate of change in the concentration of reactants or products with time. 142-45-0, Name is Acetylenedicarboxylic Acid, formurla is C4H2O4. In a document, author is Huang, Mei, introducing its new discovery. COA of Formula: C4H2O4.

The novel alpha 7 nicotinic acetylcholine receptor agonist EVP-6124 enhances dopamine, acetylcholine, and glutamate efflux in rat cortex and nucleus accumbens

Background Alpha7 and alpha 4 beta 2 nicotinic acetylcholine receptor (nAChR) agonists have been shown to improve cognition in various animal models of cognitive impairment and are of interest as treatments for schizophrenia, Alzheimer’s disease, and other cognitive disorders. Increased release of dopamine (DA), acetylcholine (ACh), glutamate (Glu), and gamma-aminobutyric acid (GABA) in cerebral cortex, hippocampus, and nucleus accumbens (NAC) has been suggested to contribute to their beneficial effects on cognition. Results Using in vivo microdialysis, we found that EVP-6124 [(R)-7-chloro-N-quinuclidin-3-yl) benzo[b] thiophene-2-carboxamide], a high-affinity alpha 7 nAChR partial agonist, at 0.1 mg/kg, s.c., increased DA efflux in the medial prefrontal cortex (mPFC) and NAC. EVP-6124, 0.1 and 0.3 mg/kg, also increased efflux of ACh in the mPFC but not in the NAC. Similarly, EVP-6124, 0.1 mg/kg, but not 0.03 and 0.3 mg/kg, significantly increased mPFC Glu efflux. Thus, EVP-6124 produced an inverted U-shaped curve for DA and Glu release, as previously reported for other alpha 7 nAChR agonists. The three doses of EVP-6124 did not produce a significant effect on GABA efflux in either region. Pretreatment with the selective alpha 7 nAChR antagonist, methyllycaconitine (MLA, 1.0 mg/kg), significantly blocked cortical DA and Glu efflux induced by EVP-6124 (0.1 mg/kg), suggesting that the effects of EVP-6124 on these neurotransmitters were due to alpha 7 nAChR agonism. MLA only partially blocked the effects of EVP-6124 on ACh efflux in the mPFC. Conclusion These results suggest increased cortical DA, ACh, and Glu release, which may contribute to the ability of the alpha 7 nAChR agonist, EVP-6124, to treat cognitive impairment and possibly other dimensions of psychopathology.

If you are hungry for even more, make sure to check my other article about 142-45-0, COA of Formula: C4H2O4.

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

Related Products of 123-96-6, The transformation of simple hydrocarbons into more complex and valuable products via catalytic C¨CH bond functionalisation has revolutionised modern synthetic chemistry. 123-96-6, Name is Octan-2-ol, SMILES is CC(O)CCCCCC, belongs to quinuclidines compound. In a article, author is BESIDSKY, Y, introduce new discover of the category.

SYNTHESIS AND REACTIVITY OF 6-CARBAMOYL-5-PHENYL-2,3,5,6-TETRAHYDRO-1H-1,4-ETHANOBENZO[F]QUINOLINE – X-RAY MOLECULAR-STRUCTURE OF (4AR-ASTERISK,5S-ASTERISK,6R-ASTERISK,10BR-ASTERISK)-5-PHENYL-2,3,4A,5,6,10B-HEXAHYDRO-1H-1,4-ETHANOBENZO[F]QUINOLIN-6-YL ACETATE

Cyclocondensation of 2-(2-cyano-1,2-diphenylethyl)quinuclidin-3-one 1 in the presence of sulfuric acid gave an intramolecular phenylation instead of lactam formation. The cyclic product was hydrogenated to give 6-carbamoyl-5-phenyl-2,3,4a,5,6,10b-hexahydro-1H-1,4-ethanobenzo- [f]quinoline. On treatment with LiAIH(4) the carbamoyl group was stereospecifically replaced by a hydroxy group. The alcohol was acetylated and the structure was confirmed by X-ray crystallography. The hydroxylation reaction is believed to proceed via a carbonitrile intermediate. In the presence of air the nitrile can be converted to a ketone which is then reduced to the alcohol with an overall retention of configuration.

Related Products of 123-96-6, 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.I hope my blog about 123-96-6 is helpful to your research.

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

Application of 5392-40-5, Enzymes are biological catalysts that produce large increases in reaction rates and tend to be specific for certain reactants and products. 5392-40-5, Name is 3,7-Dimethylocta-2,6-dienal, SMILES is C/C(C)=CCC/C(C)=C/C=O, belongs to quinuclidines compound. In a article, author is Primozic, Ines, introduce new discover of the category.

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)

Application of 5392-40-5, Enzymes are biological catalysts that produce large increases in reaction rates and tend to be specific for certain reactants and products. I hope my blog about 5392-40-5 is helpful to your research.

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

Chemistry can be defined as the study of matter and the changes it undergoes. You¡¯ll sometimes hear it called the central science because it is the connection between physics and all the other sciences, starting with biology. 4771-80-6, Name is Cyclohex-3-enecarboxylic acid, molecular formula is , belongs to quinuclidines compound. In a document, author is Venkateswaran, Amudhan, COA of Formula: C7H10O2.

Antiangiogenic properties of substituted (Z)-(+/-)-2-(N-benzylindol-3-ylmethylene)quinuclidin-3-ol/one analogs and their derivatives

In the past half century research efforts have defined a critical role for angiogenesis in tumor growth and metastasis. We previously reported that inhibition of a novel target, ENOX1, by a (Z)-2-benzylindol-3-ylmethylene) quinuclidin-3-ol, suppressed tumor angiogenesis. The present study was undertaken in order to establish structure-activity relationships for quinuclidine analogs. The angiogenesis inhibiting activity of a series of substituted (Z)-(+/-)-2-(N-benzylindol-3-ylmethylene)quinuclidin-3-ols (1a-1k), (Z)-2-benzylindol-3-ylmethylene) quinuclidin-3-ones (2a-2h), (Z)-(+/-)-2-(1H/N-methyl-indol-3-ylmethylene) quinuclidin-3-ols (3a-3b), and substituted (Z)-(+/-)-2-(N-benzenesulfonylindol-3-yl-methylene) quinuclidin-3-ols and their derivatives (4a-4d) that incorporate a variety of substituents in both the indole and N-benzyl moieties was evaluated using Human Umbilical Vein Endothelial Cells (HUVECs) subjected to in vitro cell migration scratch assays, tubule formation in Matrigel, cell viability and proliferation assays. In total, 25 different analogs were evaluated. Based on in vitro cell migration scratch assays, eight analogs were identified as potent angiogenesis inhibitors at 10 mu M, a concentration that was determined to be nontoxic by colony formation assay. In addition, this approach identified a potent antiangiogenic ENOX1 inhibitor, analog 4b. (C) 2010 Elsevier Ltd. All rights reserved.

Sometimes chemists are able to propose two or more mechanisms that are consistent with the available data. If a proposed mechanism predicts the wrong experimental rate law, however, the mechanism must be incorrect.Welcome to check out more blogs about 4771-80-6, in my other articles. COA of Formula: C7H10O2.

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

In an article, author is Ugawa, T, once mentioned the application of 765-70-8, Formula: C6H8O2, Name is 3-Methylcyclopentane-1,2-dione, molecular formula is C6H8O2, molecular weight is 112.13, MDL number is MFCD00001417, category is quinuclidines. Now introduce a scientific discovery about this category.

Effect of YM-53601, a novel squalene synthase inhibitor, on the clearance rate of plasma LDL and VLDL in hamsters

1 To better understand how it decreases plasma cholesterol and triglyceride, we evaluated the effect of YM-53601 ((E-2-[2-fluoro-2-(quinuclidin-3-ylidene) ethoxy]-9H-carbozole monohydrochloride) on the clearance rate of low density lipoprotein (LDL) and very low density lipoprotein (VLDL) in hamsters. 2 Treatment with YM-53601 at 50 mg kg(-1) for 5 days in hamsters fed a normal diet enhanced the disappearance of 1,1′-Dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanine perchlorate (DiI)-VLDL and DiI-LDL. This effect on DiI-LDL was lost in the early phase after DiI-methyl(met)-LDL, chemically modified to block LDL receptor binding, was injected in hamsters, but was retained in the late phase. Pre-treatment with prolamine sulphate, which inhibits the activity of LPL, also failed to enhance DiI-VLDL clearance rate by YM-53601. 3 Even on single oral administration at 30 mg kg(-1), YM-53601 enhanced the disappearance of the high concentration of plasma triglyceride after injection of intrafat, an emulsion of fat. Plasma triglyceride was significantly decreased as soon as 1 h after single administration of YM-53601 in hamsters fed a normal diet. 4 These results indicate that the decrease in plasma total cholesterol and triglyceride after the treatment with YM-53601 is due to its enhancement of the clearance rate of LDL and VLDL, respectively. Moreover, YM-53601 may be effective in decreasing plasma triglyceride levels early in the course of treatment of hypertriglyceridaemia in humans.

If you are interested in 765-70-8, you can contact me at any time and look forward to more communication. Formula: C6H8O2.

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

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, 502-49-8, Name is Cyclooctanone, SMILES is O=C1CCCCCCC1, in an article , author is Primozic, Ines, once mentioned of 502-49-8, Product Details of 502-49-8.

Preparation of Novel meta- and para-Substituted N-Benzyl Protected Quinuclidine Esters and Their Resolution with Butyrylcholinesterase

Since the optically active quinuclidin-3-ol is an important intermediate in the preparation of physiologically or pharmacologically active compounds, a new biocatalytic method for the production of chiral quinuclidin-3-ols was examined. Butyrylcholinesterase (BChE; EC 3.1.1.8) was chosen as a biocatalyst in a preparative kinetic resolution of enantiomers. A series of racemic, (R)- and (S)-esters of quinuclidin-3-ol and acetic, benzoic, phthalic and isonicotinic acids were synthesized, as well as their racemic quaternary N-benzyl, meta- and para-N-bromo and N-methylbenzyl derivatives. After the resolution, all N-benzyl protected groups were successfully removed by catalytic transfer hydrogenation with ammonium formate (10% Pd-C). Hydrolyses studies with BChE confirmed that (R)-enantiomers of the prepared esters are much better substrates for the enzyme than (S)-enantiomers. Introduction of bromine atom or methyl group in the meta or para position of the benzyl moiety resulted in a considerable improvement of the stereoselectivity compared to the non-substituted compounds. Optically pure quinuclidin-3-ols were prepared in high yields and enantiopurity by the usage of various N-benzyl protected groups and BChE as a biocatalyst.

But sometimes, even after several years of basic chemistry education, it is not easy to form a clear picture on how they govern reactivity! 502-49-8, you can contact me at any time and look forward to more communication. Product Details of 502-49-8.

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

Application of 5392-40-5, Catalysts allow a reaction to proceed via a pathway that has a lower activation energy than the uncatalyzed reaction. 5392-40-5, Name is 3,7-Dimethylocta-2,6-dienal, SMILES is C/C(C)=CCC/C(C)=C/C=O, belongs to quinuclidines compound. In a article, author is Odzak, Renata, introduce new discover of the category.

3-Amidoquinuclidine derivatives: Synthesis and interaction with butyrylcholinesterase

Racemates as well as (R)- and (S)-enantiomers of 3-pivalamidoquinuclidine (PivQ) and 3-acetamidoquinuclidine (AcQ) were prepared. Their quaternary racemic and enantiomerically pure N-benzyl derivatives (BnlPivQ and BnlAcQ) were synthesized as well. The amides were tested as substrates and inhibitors of butyrylcholinesterase (BChE) from horse serum (EC 3.1.1.8). No hydrolysis was observed under the experimental conditions applied. On the contrary, inhibition of BChE by (R)- and (S)-enantiomers of N-benzylquinuclidinium amides of pivalic acid was observed. The (S)-BnlPivQ with K-i = 41.57 mu mol dm(-3) was 3-fold more potent inhibitor than the (R)-enantiomer. On the other hand, preliminary results indicated that both enantiomers of N-benzylquinuclidinum amides of acetic acid may possibly be inhibitors as well as activators depending on the concentrations of benzoylcholine (BzCh) used as a substrate of BChE.

Application of 5392-40-5, 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.I hope my blog about 5392-40-5 is helpful to your research.

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

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, 535-75-1, Name is Pipecolinic Acid, SMILES is O=C(C1NCCCC1)O, in an article , author is Tang, Cuyue, once mentioned of 535-75-1, SDS of cas: 535-75-1.

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. Interested yet? Read on for other articles about 535-75-1, you can contact me at any time and look forward to more communication. SDS of cas: 535-75-1.

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