Search results for "Cyclic S-Oxides"

showing 3 items of 3 documents

3H-1,2-benzoxathiepine 2,2-dioxides: a new class of isoform-selective carbonic anhydrase inhibitors

2017

Abstract A new chemotype with carbonic anhydrase (CA, EC 4.2.1.1) inhibitory action has been discovered, the homo-sulfocoumarins (3H-1,2-benzoxathiepine 2,2-dioxides) which have been designed considering the (sulfo)coumarins as lead molecules. An original synthetic strategy of a panel of such derivatives led to compounds with a unique inhibitory profile and very high selectivity for the inhibition of the tumour associated (CA IX/XII) over the cytosolic (CA I/II) isoforms. Although the CA inhibition mechanism with these new compounds is unknown for the moment, we hypothesize that it may be similar to that of the sulfocoumarins, i.e. hydrolysis to the corresponding sulfonic acids which therea…

Gene isoformStereochemistryHigh selectivityInhibitory postsynaptic potential01 natural sciencesStructure-Activity RelationshipHydrolysisCarbonic anhydraseDrug DiscoveryHumansMoleculeCarbonic Anhydrase InhibitorsCarbonic AnhydrasesPharmacologyCarbonic anhydraseDose-Response Relationship DrugMolecular Structurebiology010405 organic chemistryChemistrylcsh:RM1-950Active sitehomo-sulfocoumarinsGeneral MedicineCyclic S-Oxides0104 chemical sciencesinhibitor010404 medicinal & biomolecular chemistryCytosollcsh:Therapeutics. PharmacologyBiochemistrysulfocoumarinbiology.proteinResearch PaperJournal of Enzyme Inhibition and Medicinal Chemistry
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Inhibition of VEGF expression through blockade of Hif1a and STAT3 signalling mediates the anti-angiogenic effect of melatonin in HepG2 liver cancer c…

2013

Background: Hepatocellular carcinoma (HCC) growth relies on angiogenesis via vascular endothelial growth factor (VEGF) release. Hypoxia within tumour environment leads to intracellular stabilisation of hypoxia inducible factor 1 alpha (Hif1α) and signal transducer and activator of transcription (STAT3). Melatonin induces apoptosis in HCC, and shows anti-angiogenic features in several tumours. In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate the anti-angiogenic effects of melatonin. Methods: HepG2 cells were treated with melatonin under normoxic or CoCl2-induced hypoxia. Gene expression was analysed by RT–qPCR and western blot. Melatonin-induced anti-…

STAT3 Transcription FactorTranscriptional ActivationVascular Endothelial Growth Factor ACancer ResearchCarcinoma HepatocellularTranscription GeneticAngiogenesisAngiogenesis InhibitorsApoptosismelatoninP300-CBP Transcription FactorsHif1αBiologyMelatoninSTAT3chemistry.chemical_compoundHypoxia-Inducible Factor 1-AlphamedicineHuman Umbilical Vein Endothelial CellsHumansp300-CBP Transcription FactorsSTAT3Promoter Regions GeneticTube formationNeovascularization PathologicLiver NeoplasmsCobaltHep G2 Cellshepatocellular carcinomaHypoxia-Inducible Factor 1 alpha SubunitVEGFCell Hypoxiadigestive system diseasesCyclic S-OxidesVascular endothelial growth factorGene Expression Regulation NeoplasticVascular endothelial growth factor AOncologychemistryCancer researchbiology.proteinTranslational Therapeuticsmedicine.drugSignal Transduction
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Genome-Wide Inhibition of Pro-atherogenic Gene Expression by Multi-STAT Targeting Compounds as a Novel Treatment Strategy of CVDs.

2018

Cardiovascular diseases (CVDs), including atherosclerosis, are globally the leading cause of death. Key factors contributing to onset and progression of atherosclerosis include the pro-inflammatory cytokines Interferon (IFN)a and IFN? and the Pattern Recognition Receptor (PRR) Toll-like receptor 4 (TLR4). Together, they trigger activation of Signal Transducer and Activator of Transcription (STAT)s. Searches for compounds targeting the pTyr-SH2 interaction area of STAT3, yielded many small molecules, including STATTIC and STX-0119. However, many of these inhibitors do not seem STAT3-specific. We hypothesized that multi-STAT-inhibitors that simultaneously block STAT1, STAT2, and STAT3 activit…

lcsh:Immunologic diseases. Allergy0301 basic medicineMaleIn silicoImmunologyGene ExpressionBiologystatIn silico dockingCell LineSmall Molecule Librariessrc Homology Domains03 medical and health sciencesCVDs treatment strategyImmunology and AllergyAnimalsHumansvascular inflammationSTAT1STAT2STAT3Vascular inflammationCells CulturedOriginal ResearchOxadiazolesGene Expression ProfilingSTATPattern recognition receptorin silico dockingFarmaciaAtherosclerosisCyclic S-OxidesMice Inbred C57BLSTAT Transcription Factors030104 developmental biologyCardiovascular DiseasesTLR4biology.proteinSTAT proteinCancer researchQuinolinesmulti-STAT inhibitorsMulti-STAT inhibitorslcsh:RC581-607Genome-Wide Association StudySignal TransductionFrontiers in immunology
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