Category: 637-07-0

Lin, Chingju published the artcileFenofibrate inhibits hypoxia-inducible factor-1 alpha and carbonic anhydrase expression through activation of AMP-activated protein kinase/ HO -1/Sirt1 pathway in glioblastoma cells, Application of Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, the publication is Environmental Toxicology (2021), 36(12), 2551-2561, database is CAplus and MEDLINE.

Cancer and its associated conditions have significant impacts on public health at many levels worldwide, and cancer is the leading cause of death among adults. Peroxisome proliferator-activated receptor α (PPARα)-specific agonists, fibrates, have been approved by the Food and Drug Administration for managing hyperlipidemia. PPARα-specific agonists exert anti-cancer effects in many human cancer types, including glioblastoma (GBM). Recently, we have reported that the hypoxic state in GBM stabilizes hypoxia-inducible factor-1 alpha (HIF-1α), thus contributing to tumor escape from immune surveillance by activating the expression of the pH-regulating protein carbonic anhydrase IX (CA9). In this study, we aimed to study the regulatory effects of the PPARα agonist fibrate on the regulation of HIF-1α expression and its downstream target protein in GBM. Our findings showed that fenofibrate is the high potency compound among the various fibrates that inhibit hypoxia-induced HIF-1α and CA9 expression in GBM. Moreover, fenofibrate-inhibited HIF-1α expression is mediated by HO-1 activation in GBM cells through the AMP-activated protein kinase (AMPK) pathway. In addition, fenofibrate-enhanced HO-1 upregulation activates SIRT1 and leads to subsequent accumulation of SIRT1 in the nucleus, which further promotes HIF-1α deacetylation and inhibits CA9 expression. Using a protein synthesis inhibitor, cycloheximide, we also observed that fenofibrate inhibited HIF-1α protein synthesis. In addition, the administration of the proteasome inhibitor MG132 showed that fenofibrate promoted HIF-1α protein degradation in GBM. Hence, our results indicate that fenofibrate is a useful anti-GBM agent that modulates hypoxia-induced HIF-1α expression through multiple cellular pathways.

Environmental Toxicology published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C12H15ClO3, Application of Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate.

Referemce:
https://en.wikipedia.org/wiki/Chloride,
Chlorides – an overview | ScienceDirect Topics

Derhamine, Sary Abou published the artcileNickel-Catalyzed Mono-Selective α-Arylation of Acetone with Aryl Chlorides and Phenol Derivatives, Recommanded Product: Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, the publication is Angewandte Chemie, International Edition (2020), 59(43), 18948-18953, database is CAplus and MEDLINE.

The challenging nickel-catalyzed mono-α-arylation of acetone with aryl chlorides, pivalates, and carbamates was achieved for the first time. A nickel/Josiphos-based catalytic system is shown to feature unique catalytic behavior, allowing the highly selective formation of the desired mono-α-arylated acetone. The developed methodol. was applied to a variety of (hetero)aryl chlorides including biol. relevant derivatives The methodol. was extended to the unprecedented coupling of acetone with phenol derivatives Mechanistic studies allowed the isolation and characterization of key Ni⁰ and Ni^II catalytic intermediates. The Josiphos ligand is shown to play a key role in the stabilization of Ni^II intermediates to allow a Ni⁰/Ni^II catalytic pathway. Mechanistic understanding was then leveraged to improve the protocol using an air-stable Ni^II pre-catalyst.

Angewandte Chemie, International Edition published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C12H15ClO3, Recommanded Product: Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate.

Referemce:
https://en.wikipedia.org/wiki/Chloride,
Chlorides – an overview | ScienceDirect Topics

Duesel, Simon Josef Siegfried published the artcileOxidative Photochlorination of Electron-Rich Arenes via in situ Bromination, Application In Synthesis of 637-07-0, the publication is European Journal of Organic Chemistry (2020), 2020(10), 1491-1495, database is CAplus.

Electron-rich arenes are oxidatively photochlorinated in the presence of catalytic amounts of bromide ions, visible light, and 4CzIPN as organic photoredox catalyst. The substrates are brominated in situ in a first photoredox-catalyzed oxidation step, followed by a photocatalyzed ipso-chlorination, yielding the target compounds in high ortho/para regioselectivity. Dioxygen serves as a green and convenient terminal oxidant. The use of aqueous hydrochloric acid as the chloride source reduces the amount of saline byproducts.

European Journal of Organic Chemistry published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C12H15ClO3, Application In Synthesis of 637-07-0.

Referemce:
https://en.wikipedia.org/wiki/Chloride,
Chlorides – an overview | ScienceDirect Topics

Tony, D. Eswar published the artcileA comparative research between pharmacological and nonpharmacological profile of anti-hyperlipidemic activity on rodents, HPLC of Formula: 637-07-0, the publication is Journal of Drug Delivery and Therapeutics (2021), 11(5), 65-70, database is CAplus.

The condition of hyperlipidemia is found to be a great establisher for all the neg. health consequences which may lead to cardiac complications. Continuous usage of medication alone is not permanent remedy but also need phys. exercise. The same situation was established in animals to assess the performance of pharmacol. and nonpharmacol. profile by standardized screening using In-vivo methods. The highcholesterol diet caused a significant increase in total lipids, total cholesterol (TC), total triglycerides (TG), low-d. lipoprotein cholesterol (LDL-C), and the atherogenic index, whereas the level of high-d. lipoprotein cholesterol (HDL-C) was significantly decreased for the treatment groups intended for phys. exercise. This article enables the importance of health benefited by phys. performance by depicting the biochem. parameters.

Journal of Drug Delivery and Therapeutics published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C14H26O2, HPLC of Formula: 637-07-0.

Referemce:
https://en.wikipedia.org/wiki/Chloride,
Chlorides – an overview | ScienceDirect Topics

Boodhoo, Nitish published the artcileGlutaminolysis and glycolysis are essential for optimal replication of Marek’s disease virus, Name: Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, the publication is Journal of Virology (2020), 94(4), e01680-19, database is CAplus and MEDLINE.

Marek’s disease virus causes a deadly lymphoproliferative disease in chickens and modulates metabolism of host cells. Metabolic anal. of MDV-infected chicken embryonic fibroblasts identified elevated levels of metabolites involved in glutamine catabolism, such as glutamic acid, alanine, glycine, pyrimidine, and creatine. In addition, our results demonstrate that glutamine uptake is elevated by MDV-infected cells in vitro. Although glutamine, but not glucose, deprivation significantly reduced cell viability in MDV-infected cells, both glutamine and glucose were required for virus replication and spread. In the presence of min. glutamine requirements based on optimal cell viability, virus replication was partially rescued by the addition of the tricarboxylic acid (TCA) cycle intermediate, α-ketoglutarate, suggesting that exogenous glutamine is an essential carbon source for the TCA cycle to generate energy and macromols. required for virus replication. Surprisingly, the inhibition of CPT1a, which is elevated in MDV-infected cells, by chem. (etomoxir) or physiol. (malonyl-CoA) inhibitors, did not reduce MDV replication, indicating that MDV replication does not require fatty acid β-oxidation Taken together, our results demonstrate that MDV infection activates anaplerotic substrate from glucose to glutamine to provide energy and macromols. required for MDV replication, and optimal MDV replication occurs when the cells do not depend on mitochondrial β-oxidation

Journal of Virology published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C12H15ClO3, Name: Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate.

Referemce:
https://en.wikipedia.org/wiki/Chloride,
Chlorides – an overview | ScienceDirect Topics

Chen, Yih-Ting published the artcileAcute kidney disease and acute kidney injury biomarkers in coronary care unit patients, Product Details of C12H15ClO3, the publication is BMC Nephrology (2020), 21(1), 207, database is CAplus and MEDLINE.

Background: Acute kidney disease (AKD) describes acute or subacute damage and/or loss of kidney function for a duration of between 7 and 90 days after exposure to an acute kidney injury (AKI) initiating event. This study investigated the predictive ability of AKI biomarkers in predicting AKD in coronary care unit (CCU) patients. Methods: A total of 269 (mean age: 64 years; 202 (75%) men and 67 (25%) women) patients admitted to the CCU of a tertiary care teaching hospital from Nov. 2009 to Sept. 2014 were enrolled. Information considered necessary to evaluate 31 demog., clin. and laboratory variables (including AKI biomarkers) was prospectively recorded on the first day of CCU admission for post hoc anal. as predictors of AKD. Blood and urinary samples of the enrolled patients were tested for neutrophil gelatinase-associated lipocalin (NGAL), cystatin C (CysC) and interleukin-18 (IL-18). Results: The overall hospital mortality rate was 4.8%. Of the 269 patients, 128 (47.6%) had AKD. Multivariate logistic regression anal. revealed that age, Hb, ejection fraction and serum IL-18 were independent predictors of AKD. Cumulative survival rates at 5 years of follow-up after hospital discharge differed significantly (p < 0.001) between subgroups of patients diagnosed with AKD (stage 0A, 0C, 1, 2 and 3). The overall 5-yr survival rate was 81.8% (220/269). Multivariate Cox proportional hazard anal. revealed that urine NGAL, body weight and Hb level were independent risk factors for 5-yr mortality. Conclusions: This investigation confirmed that AKI biomarkers can predict AKD in CCU patients. Age, Hb, ejection fraction and serum IL-18 were independently associated with developing AKD in the CCU patients, and urine NGAL, body weight and Hb level could predict 5-yr survival in these patients.

BMC Nephrology published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C12H15ClO3, Product Details of C12H15ClO3.

Referemce:
https://en.wikipedia.org/wiki/Chloride,
Chlorides – an overview | ScienceDirect Topics

Liu, Yan published the artcileIdentification of a hormone response element that mediates suppression of APOF by LXR and PPARα agonists, Synthetic Route of 637-07-0, the publication is Biochimica et Biophysica Acta, Molecular and Cell Biology of Lipids (2020), 1865(3), 158583, database is CAplus and MEDLINE.

Here we show in human liver C3A cells that APOF mRNA levels are reduced by agonists of LXR and PPARα nuclear receptors. This neg. regulation requires co-incubation with the RXR agonist, retinoic acid. Bioinformatic anal. of the ∼2 kb sequence upstream of the APOF promoter identified one potential LXR and 4 potential PPARα binding sites clustered between nucleotides -2007 and -1961. ChIP anal. confirmed agonist-dependent binding of LXRα, PPARα, and RXRα to this hormone response element complex (HREc). A luciferase reporter containing the 2 kb 5′ APOF sequence was neg. regulated by LXR and PPARα ligands as seen in cells. This regulation was maintained in constructs lacking the ∼1700 nucleotides between the HREc and the APOF proximal promoter. Mutations of the HREc that disrupted LXRα and PPARα binding led to the loss of reporter construct inhibition by agonists of these nuclear receptors. siRNA knockdown studies showed that APOF gene regulation by LXRα or PPARα agonists did not require an interaction between these two nuclear receptors. Thus, APOF is subject to neg. regulation by agonist-activated LXR or PPARα nuclear receptors binding to a regulatory element ∼1900 bases 5′ to the APOF promoter. High fat, cholesterol-enriched diets likely reduce APOF gene expression via these receptors interacting at this regulatory site.

Biochimica et Biophysica Acta, Molecular and Cell Biology of Lipids published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C12H15ClO3, Synthetic Route of 637-07-0.

Referemce:
https://en.wikipedia.org/wiki/Chloride,
Chlorides – an overview | ScienceDirect Topics

Wang, Weijin published the artcileNitromethane-enabled fluorination of styrenes and arenes, Product Details of C12H15ClO3, the publication is CCS Chemistry (2020), 2(6), 566-575, database is CAplus.

Herein, nitromethane (MeNO₂) as an efficient activator of Selectfluor and NFSI, as well as a stabilizer of carbocations was disclosed. Therefore, the fluoro-azidation, fluoroamination, fluoroesterification of styrenes, and C-H fluorination of (hetero)arenes were well realized just by the facilitation of MeNO₂. The mild reaction conditions and practicability made our current method a versatile protocol for accessing organofluorides.

CCS Chemistry published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C12H10FeO4, Product Details of C12H15ClO3.

Referemce:
https://en.wikipedia.org/wiki/Chloride,
Chlorides – an overview | ScienceDirect Topics

Johnson, Joshua L. published the artcileOptimal pH 8.5 to 9 for the hydrolysis of vixotrigine and other basic substrates of carboxylesterase-1 in human liver microsomes, Quality Control of 637-07-0, the publication is Xenobiotica (2022), 52(2), 105-112, database is CAplus and MEDLINE.

Vixotrigine is a voltage- and use-dependent sodium channel blocker under investigation for the potential treatment of neuropathic pain. One of the major in vivo metabolic pathways of vixotrigine in humans is the hydrolysis of the carboxamide to form the carboxylic acid metabolite M14. The in vitro formation of M14 in human hepatocytes was inhibited by the carboxylesterase (CES) inhibitor Bis(4-nitrophenyl) phosphate in a concentration-dependent manner. The hydrolysis reaction was identified to be catalyzed by recombinant human CES1b. Initial observation of only trace level formation of M14 in human liver microsomes at pH 7.4 caused us to doubt the involvement of CES1, an enzyme localised at the endoplasmic reticulum and the dominant carboxylesterase in human liver. Further investigation has revealed that optimal pH for the hydrolysis of vixotrigine and two other basic substrates of CES1, methylphenidate and oseltamivir, in human liver microsomes was pH 8.5-9 which is higher than their resp. pKa(base), suggesting that neutral form of basic substrates is probably preferred for CES1 catalysis in liver microsomes.

Xenobiotica published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C12H15ClO3, Quality Control of 637-07-0.

Referemce:
https://en.wikipedia.org/wiki/Chloride,
Chlorides – an overview | ScienceDirect Topics

Gevorgyan, Ashot published the artcileFormal C-H Carboxylation of Unactivated Arenes, SDS of cas: 637-07-0, the publication is Chemistry – A European Journal (2020), 26(27), 6064-6069, database is CAplus and MEDLINE.

A formal C-H carboxylation of unactivated arenes e.g., I using CO₂ in green solvents is described. The present strategy combines a sterically controlled Ir-catalyzed C-H borylation followed by a Cu-catalyzed carboxylation of the in situ generated organoboronates. The reaction is highly regioselective for the C-H carboxylation of unactivated arenes e.g., I (1,3-disubstituted and 1,2,3-trisubstituted benzenes, 1,2- or 1,4-sym. substituted benzenes, fluorinated benzenes and different heterocycles). The developed methodol. was applied to the late-stage C-H carboxylation of com. drugs and ligands.

Chemistry – A European Journal published new progress about 637-07-0. 637-07-0 belongs to chlorides-buliding-blocks, auxiliary class Inhibitor,Cell Cycle,PPAR, name is Ethyl 2-(4-chlorophenoxy)-2-methylpropanoate, and the molecular formula is C12H15ClO3, SDS of cas: 637-07-0.

Referemce:
https://en.wikipedia.org/wiki/Chloride,
Chlorides – an overview | ScienceDirect Topics