Category: 5291-32-7

An article , which mentions 5291-32-7, molecular formula is C10H17NO3. The compound – APR-246 played an important role in people’s production and life., Product Details of 5291-32-7

SLMP53-2 restoreswild-type-like function to mutant p53 through hsp70: Promising activity in hepatocellular carcinoma

Half of human cancers harbor TP53 mutations that render p53 inactive as a tumor suppressor. In these cancers, reactivation of mutant p53 (mutp53) through restoration of wild-type-like function constitutes a valuable anticancer therapeutic strategy. In order to search for mutp53 reactivators, a small library of tryptophanol-derived oxazoloisoindolinones was synthesized and the potential of these compounds as mutp53 reactivators and anticancer agents was investigated in human tumor cells and xenograft mouse models. By analysis of their anti-proliferative effect on a panel of p53-null NCI-H1299 tumor cells ectopically expressing highly prevalent mutp53, the compound SLMP53-2 was selected based on its potential reactivation of multiple structuralmutp53. In mutp53-Y220C-expressing hepatocellular carcinoma (HCC) cells, SLMP53-2-induced growth inhibition was mediated by cell cycle arrest, apoptosis, and endoplasmic reticulum stress response. In these cells, SLMP53-2 restored wild-type-like conformation and DNA-binding ability of mutp53-Y220C by enhancing its interaction with the heat shock protein 70 (Hsp70), leading to the reestablishment of p53 transcriptional activity. Additionally, SLMP53-2 displayed synergistic effect with sorafenib, the only approved therapy for advanced HCC. Notably, it exhibited potent antitumor activity in human HCC xenograft mouse models with a favorable toxicological profile. Collectively, SLMP53-2 is a new mutp53-targeting agent with promising antitumor activity, particularly against HCC.

Balanced chemical reaction does not necessarily reveal either the individual elementary reactions by which a reaction occurs or its rate law.Product Details of 5291-32-7. In my other articles, you can also check out more blogs about 5291-32-7

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Quinuclidine – Wikipedia,
Quinuclidine | C7H169N | ChemSpider

Chemistry is traditionally divided into organic and inorganic chemistry. Product Details of 5291-32-7, 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

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).

Because enzymes can increase reaction rates by enormous factors and tend to be very specific, Product Details of 5291-32-7, typically producing only a single product in quantitative yield, they are the focus of active research.you can also check out more blogs about Product Details of 5291-32-7

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Quinuclidine – Wikipedia,
Quinuclidine | C7H164N | ChemSpider

Chemistry is traditionally divided into organic and inorganic chemistry. COA of Formula: C10H17NO3, 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

Piperlongumine and p53-reactivator APR-246 selectively induce cell death in HNSCC by targeting GSTP1

TP53 mutations frequently occur in head and neck squamous cell carcinoma (HNSCC) patients without human papillomavirus infection. The recurrence rate for these patients is distinctly high. It has been actively explored to identify agents that target TP53 mutations and restore wild-type (WT) TP53 activities in HNSCC. PRIMA-1 (p53-reactivation and induction of massive apoptosis-1) and its methylated analogue PRIMA-1Met (also called APR-246) were found to be able to reestablish the DNA-binding activity of p53 mutants and reinstate the functions of WT p53. Herein we report that piperlongumine (PL), an alkaloid isolated from Piper longum L., synergizes with APR-246 to selectively induce apoptosis and autophagic cell death in HNSCC cells, whereas primary and immortalized mouse embryonic fibroblasts and spontaneously immortalized non-tumorigenic human skin keratinocytes (HaCat) are spared from the damage by the co-treatment. Interestingly, PL-sensitized HNSCC cells to APR-246 are TP53 mutation-independent. Instead, we demonstrated that glutathione S-transferase pi 1 (GSTP1), a GST family member that catalyzes the conjugation of GSH with electrophilic compounds to fulfill its detoxification function, is highly expressed in HNSCC tissues. Administration of PL and APR-246 significantly suppresses GSTP1 activity, resulting in the accumulation of ROS, depletion of GSH, elevation of GSSG, and DNA damage. Ectopic expression of GSTP1 or pre-treatment with antioxidant N-acetyl-l-cysteine (NAC) abrogates the ROS elevation and decreases DNA damage, apoptosis, and autophagic cell death prompted by PL/APR-246. In addition, administration of PL and APR-246 impedes UMSCC10A xenograft tumor growth in SCID mice. Taken together, our data suggest that HNSCC cells are selectively sensitive to the combination of PL and APR-246 due to a remarkably synergistic effect of the co-treatment in the induction of ROS by suppression of GSTP1.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H170N | ChemSpider

One of the major reasons for studying chemical kinetics is to use measurements of the macroscopic properties of a system, SDS of cas: 5291-32-7, such as the rate of change in the concentration of reactants or products with time.In a article, mentioned the application of 5291-32-7, Name is APR-246, molecular formula is C10H17NO3

Aqueous solution comprising 3-quinuclidinones for the treatment of hyperproliferative, autoimmune and heart disease

no abstract published

Sometimes chemists are able to propose two or more mechanisms that are consistent with the available data. SDS of cas: 5291-32-7, If a proposed mechanism predicts the wrong experimental rate law, however, the mechanism must be incorrect.Welcome to check out more blogs about 5291-32-7, in my other articles.

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Quinuclidine | C7H163N | ChemSpider

Related Products of 5291-32-7, 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.Related Products of 5291-32-7, Name is APR-246, molecular formula is C10H17NO3, introducing its new discovery.

Mutant p53 tunes the NRF2-dependent antioxidant response to support survival of cancer cells

NRF2 (NFE2L2) is one of the main regulators of the antioxidant response of the cell. Here we show that in cancer cells NRF2 targets are selectively upregulated or repressed through a mutant p53-dependent mechanism. Mechanistically, mutant p53 interacts with NRF2, increases its nuclear presence and resides with NRF2 on selected ARE containing gene promoters activating the transcription of a specific set of genes while leading to the transcriptional repression of others. We show that thioredoxin (TXN) is a mutant p53-activated NRF2 target with pro-survival and pro-migratory functions in breast cancer cells under oxidative stress, while heme oxygenase 1 (HMOX1) is a mutant p53-repressed target displaying opposite effects. A gene signature of NRF2 targets activated by mutant p53 shows a significant association with bad overall prognosis and with mutant p53 status in breast cancer patients. Concomitant inhibition of thioredoxin system with Auranofin and of mutant p53 with APR-246 synergizes in killing cancer cells expressing p53 gain-of-function mutants.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H172N | ChemSpider

Electric Literature of 5291-32-7, 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, Electric Literature of 5291-32-7, molcular formula is C10H17NO3, introducing its new discovery.

2-SULFONYLPYRIMIDINES

The invention relates to 2-sulfonylpyrimidine compounds and salts and solvates thereof for use in the treatment of a proliferative disease such as cancers. The 2- sulfonyl-primidine compounds may be administered, either simultaneously or sequentially, with one or more pharmacologically active compounds and salts and solvates thereof such as an inhibitor of glutamate cysteine ligase. The 2- sulfonylpyrimidine compound may be represented by formula (I): (I) wherein: R1 is selected from C1-6 alkyl, C6-12 aryl, C7-18 aralkyl, 6- to 15-membered heteroaralkyl and 6- to 12-membered heterocyclylalkyl wherein each of these groups are optionally substituted with from one to three optional substituents; R2 is selected from CF3, O-C(O)-R6, C(O)R7, C(O)NHR7 and NHC(O)R7; R3 is selected from H, F, CI, Br, I, OH, C1-6 alkyl, OC1-6 alkyl, CH2F, CHF2, CF3, CN, NO2, CO2R8, C(O)NHR10, NHC(O)R10, (CH2)z-NR8R9 and (CH2)z-NH-C(=NH)-NH2; R4 is selected from H, C1-6 alkyl and CH2R11; R5 is selected from C1-6 alkyl; R6 is selected from H and C1-6 alkyl; R7 is selected from 5 to 9-membered heteroaryl groups, and phenyl wherein these groups are optionally substituted with from one to three optional substituents; and wherein the heteroaryl group is attached to the rest of compound of formula (I) by a carbon ring atom; R8 and R9 are independently selected from H, C1-6 alkyl and benzyl; R10 is selected from 5- to 9-membered heteroaryl groups, 5- and 6-membered heterocyclyl, and phenyl wherein these groups are optionally substituted with from one to three optional substituents; R11 is phenyl optionally substituted; and z is selected from an integer selected from o to 6.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H165N | 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 Recommanded Product: 5291-32-7, molcular formula is C10H17NO3, introducing its new discovery. , Recommanded Product: 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

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, Computed Properties of C10H17NO3, name is APR-246, introducing its new discovery. Computed Properties of C10H17NO3

COMBINATION CANCER THERAPIES

Drug combinations of a heteroarotinoid (e.g., SHetA2), and an Azabicyclooctan-3-one derivative (e.g., PRIMA-1 or PRIMAMET) and/or, a CDK4/6 inhibitor (e.g., Palbociclib, Abemaciclib, or Ribociclib), which are synergistically-effective as anti-cancer treatments, and kits and methods of use of such drug combinations.

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.Computed Properties of C10H17NO3, you can also check out more blogs aboutComputed Properties of C10H17NO3

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Quinuclidine – Wikipedia,
Quinuclidine | C7H162N | ChemSpider

Synthetic Route of 5291-32-7, The reaction rate of a catalyzed reaction is faster than the reaction rate of the uncatalyzed reaction at the same temperature.Synthetic Route of 5291-32-7, Name is APR-246, molecular formula is C10H17NO3. In a Article, authors is Schrader£¬once mentioned of Synthetic Route of 5291-32-7

Actionable perturbations of damage responses by TCL1/ATM and epigenetic lesions form the basis of T-PLL

T-cell prolymphocytic leukemia (T-PLL) is a rare and poor-prognostic mature T-cell malignancy. Here we integrated large-scale profiling data of alterations in gene expression, allelic copy number (CN), and nucleotide sequences in 111 well-characterized patients. Besides prominent signatures of T-cell activation and prevalent clonal variants, we also identify novel hot-spots for CN variability, fusion molecules, alternative transcripts, and progression-associated dynamics. The overall lesional spectrum of T-PLL is mainly annotated to axes of DNA damage responses, T-cell receptor/cytokine signaling, and histone modulation. We formulate a multi-dimensional model of T-PLL pathogenesis centered around a unique combination of TCL1 overexpression with damaging ATM aberrations as initiating core lesions. The effects imposed by TCL1 cooperate with compromised ATM toward a leukemogenic phenotype of impaired DNA damage processing. Dysfunctional ATM appears inefficient in alleviating elevated redox burdens and telomere attrition and in evoking a p53-dependent apoptotic response to genotoxic insults. As non-genotoxic strategies, synergistic combinations of p53 reactivators and deacetylase inhibitors reinstate such cell death execution.

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 Synthetic Route of 5291-32-7

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Quinuclidine – Wikipedia,
Quinuclidine | C7H175N | ChemSpider

Electric Literature of 5291-32-7, An article , which mentions Electric Literature of 5291-32-7, molecular formula is C10H17NO3. The compound – APR-246 played an important role in people’s production and life.

Efficacy of glutathione inhibitors for the treatment of ARID1A-deficient diffuse-type gastric cancers

ARID1A, a subunit of the SWI/SNF chromatin remodeling complex, increases the intracellular levels of glutathione (GSH) by upregulating solute carrier family 7 member 11 (SLC7A11). Diffuse-type gastric cancer is an aggressive tumor that is frequently associated with ARID1A deficiency. Here, we investigated the efficacy of GSH inhibition for the treatment of diffuse-type gastric cancer with ARID1A deficiency using ARID1A-proficient or -deficient patient-derived cells (PDCs). ARID1A-deficient PDCs were selectively sensitive to the GSH inhibitor APR-246, the GCLC inhibitor buthionine sulfoximine, and the SLC7A11 inhibitor erastin. Expression of SLC7A11, which is required for incorporation of cystine, and the basal level of GSH were lower in ARID1A-deficient than in ARID1A-proficient PDCs. Treatment with APR-246 decreased intracellular GSH levels, leading to the excessive production of reactive oxygen species (ROS), and these phenotypes are suppressed by supply of cystine and GSH compensators. Taken together, vulnerability of ARID1A-deficient gastric cancer cells to GSH inhibition is caused by decreased GSH synthesis due to diminished SLC7A11 expression. The present results suggest that GSH inhibition is a promising strategy for the treatment of diffuse-type gastric cancers with ARID1A deficiency.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H168N | ChemSpider