Tag: M.W:100-200

Chemistry is the experimental and theoretical study of materials on their properties at both the macroscopic and microscopic levels.In a patent£¬Which mentioned a new discovery about 5291-32-7, molcular formula is C10H17NO3, introducing its new discovery. , 5291-32-7

METHODS FOR MODULATING CHEMOTHERAPEUTIC CYTOTOXICITY

Disclosed herein are methods of reducing cytotoxicity of a chemotherapeutic agent to non-cancer cells by administering to a subject with cancer an effective amount of an agent that inhibits CD47 signaling and a chemotherapeutic agent. Example disclosed methods reduce cardiotoxicity of a chemotherapeutic agent. Also disclosed are methods of increasing cytotoxicity of a chemotherapeutic agent in cancer cells by administering to a subject with a tumor an effective amount of an agent that inhibits CD47 signaling and a chemotherapeutic agent. In some embodiments, the inhibitor of CD47 signaling is administered to the subject before, during, or after the administration of the chemotherapeutic agent.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H167N | ChemSpider

Chemistry is the experimental and theoretical study of materials on their properties at both the macroscopic and microscopic levels.In a patent£¬Which mentioned a new discovery about 123536-14-1, molcular formula is C7H16Cl2N2, introducing its new discovery. , 123536-14-1

Quinuclidine-substituted hetero-bicyclic aromatic compounds for the treatment of disease

The invention provides compounds of Formula I: 1wherein W0 is a bicyclic moiety and is 2These compounds may be in the form of pharmaceutical salts or compositions, may be in pure enantiomeric form or racemic mixtures, and are useful to treat diseases or conditions in which alpha7 is known to be involved.

Because enzymes can increase reaction rates by enormous factors and tend to be very specific, 123536-14-1, typically producing only a single product in quantitative yield, they are the focus of active research.you can also check out more blogs about 123536-14-1

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Quinuclidine – Wikipedia,
Quinuclidine | C7H98N | ChemSpider

5291-32-7, Chemistry is an experimental science, and the best way to enjoy it and learn about it is performing experiments.Introducing a new discovery about 5291-32-7, Name is APR-246

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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Quinuclidine – Wikipedia,
Quinuclidine | C7H171N | ChemSpider

67496-78-0, 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, 67496-78-0, molcular formula is C8H16N2, introducing its new discovery.

THIAZOLYL COMPOUNDS USEFUL AS KINASE INHIBITORS

The invention provides compounds of formula (I) and pharmaceutically acceptable salts thereof. The formula I thiazolyl compounds inhibit tyrosine kinase activity thereby making them useful as anticancer agents and for the treatment of Alzheimer’s disease

Because enzymes can increase reaction rates by enormous factors and tend to be very specific, 67496-78-0, typically producing only a single product in quantitative yield, they are the focus of active research.you can also check out more blogs about 67496-78-0

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Quinuclidine – Wikipedia,
Quinuclidine | C7H20N | ChemSpider

Chemistry is the experimental and theoretical study of materials on their properties at both the macroscopic and microscopic levels. 67496-78-0, In a patent£¬Which mentioned a new discovery about 67496-78-0

4-SUBSTITUTED QUINUCLIDINE DERIVATIVES, METHODS OF PRODUCTION, AND PHARMACEUTICAL USES THEREOF

The present invention relates to compounds and formulations capable of affecting nicotinic acetylcholine receptors (nAChRs), for example, as modulators of specific nicotinic receptor subtypes (specifically, the alpha7 nAChR subtype). The present invention also relates to methods for treating a wide variety of conditions and disorders, particularly those associated with dysfunction of the central and autonomic nervous systems.

Because enzymes can increase reaction rates by enormous factors and tend to be very specific, 67496-78-0, typically producing only a single product in quantitative yield, they are the focus of active research.you can also check out more blogs about 67496-78-0

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Quinuclidine – Wikipedia,
Quinuclidine | C7H17N | ChemSpider

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

Synthesis and biological characterization of 1,4,5,6- tetrahydropyrimidine and 2-amino-3,4,5,6-tetrahydropyridine derivatives as selective m1 agonists

Previous studies identified several novel tetrahydropyrimidine derivatives exhibiting muscarinic agonist activity in rat brain. Such compounds might be useful in treating cognitive and memory deficits associated with low acetylcholine levels, as found in Alzheimer’s disease. To determine the molecular features of ligands important for binding and activity at muscarinic receptor subtypes, the series of tetrahydropyrimidines was extended. Several active compounds were examined further for functional selectivity through biochemical studies of muscarinic receptor activity using receptor subtypes expressed in cell lines. Several amidine derivatives displayed high efficacy at m1 receptors and lower activity at m3 receptors coupled to phosphoinositide (PI) metabolism in A9 L cells. Four ligands, including 1b, 1f, 2b, and 7b, exhibited marked functional selectivity for m1 vs m3 receptors. Compound 1f also exhibited low activity at m2 receptors coupled to the inhibition of adenylyl cyclase in A9 L cells. Molecular modeling studies also were initiated to help understand the nature of the interaction of muscarinic agonists with the m1 receptor using a nine amino model of the m1 receptor. Several important interactions were identified, including interactions between the ester moiety and Thr192. Additional interactions were found for oxadiazoles and alkynyl derivatives with Asn382, suggesting that enhanced potency and selectivity may be achieved by maximizing interactions with Asp105, Thr192, and Ash382. Taken together, the data indicate that several amidine derivatives display functional selectivity for m1 muscarinic receptors, warranting further evaluation as therapeutic agents for the treatment of Alzheimer’s disease. In addition, several amino acid residues were identified as potential binding sites for m1 agonists. These data may be useful in directing efforts to develop even more selective m1 agonists.

Sometimes chemists are able to propose two or more mechanisms that are consistent with the available data. 827-61-2, If a proposed mechanism predicts the wrong experimental rate law, however, the mechanism must be incorrect.Welcome to check out more blogs about 827-61-2, in my other articles.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H72N | ChemSpider

5291-32-7, Chemistry is traditionally divided into organic and inorganic chemistry. The former is the study of compounds containing at least one carbon-hydrogen bonds.In a patent£¬Which mentioned a new discovery about 5291-32-7

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.

One of the oldest and most widely used commercial enzyme inhibitors is aspirin, 5291-32-7, which selectively inhibits one of the enzymes involved in the synthesis of molecules that trigger inflammation. you can also check out more blogs about 5291-32-7

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Quinuclidine – Wikipedia,
Quinuclidine | C7H166N | ChemSpider

67496-78-0, In homogeneous catalysis, the catalyst is in the same phase as the reactant. The number of collisions between reactants and catalyst is at a maximum.In a patent, 67496-78-0, name is Quinuclidin-4-ylmethanamine, introducing its new discovery.

INDOLONES USEFUL AS SEROTONERGIC AGENTS

This invention relates to compounds of the formula: STR1 which are useful as 5-HT 4 agonists or antagonists and 5-HT 3 antagonists.

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.67496-78-0, you can also check out more blogs about67496-78-0

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Quinuclidine – Wikipedia,
Quinuclidine | C7H13N | ChemSpider

827-61-2, In an article, published in an article,authors is Burns, Sean M., once mentioned the application of 827-61-2, Name is Quinuclidin-3-yl acetate,molecular formula is C9H15NO2, is a conventional compound. this article was the specific content is as follows.

High-throughput luminescent reporter of insulin secretion for discovering regulators of pancreatic Beta-cell function

Defects in insulin secretion play a central role in the pathogenesis of type 2 diabetes, yet the mechanisms driving beta-cell dysfunction remain poorly understood, and therapies to preserve glucose-dependent insulin release are inadequate. We report a luminescent insulin secretion assay that enables large-scale investigations of beta-cell function, created by inserting Gaussia luciferase into the C-peptide portion of proinsulin. Beta-cell lines expressing this construct cosecrete luciferase and insulin in close correlation, under both standard conditions or when stressed by cytokines, fatty acids, or ER toxins. We adapted the reporter for high-throughput assays and performed a 1,600-compound pilot screen, which identified several classes of drugs inhibiting secretion, as well as glucose-potentiated secretagogues that were confirmed to have activity in primary human islets. Requiring 40-fold less time and expense than the traditional ELISA, this assay may accelerate the identification of pathways governing insulin secretion and compounds that safely augment beta-cell function in diabetes.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H49N | ChemSpider

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, authors is Sheardown, Malcolm J.£¬once mentioned of 827-61-2

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, gridshock, 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-tetrahydro-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]pirenzepine binding and for their functional selectivity at pharmacologic 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 methscopolamine (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.

A reaction mechanism is the microscopic path by which reactants are transformed into products. Each step is an elementary reaction. In my other articles, you can also check out more blogs about 827-61-2

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Quinuclidine – Wikipedia,
Quinuclidine | C7H83N | ChemSpider