Search results for "Structure-Activity relationship"

showing 10 items of 743 documents

Nonacidic Farnesoid X Receptor Modulators.

2017

As a cellular bile acid sensor, farnesoid X receptor (FXR) participates in regulation of bile acid, lipid and glucose homeostasis, and liver protection. Clinical results have validated FXR as therapeutic target in hepatic and metabolic diseases. To date, potent FXR agonists share a negatively ionizable function that might compromise their pharmacokinetic distribution and behavior. Here we report the development and characterization of a high-affinity FXR modulator not comprising an acidic residue.

0301 basic medicineMalemedicine.drug_classPyridinesPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearATP-binding cassette transporterCholesterol 7 alpha-hydroxylase01 natural sciencesRats Sprague-Dawley03 medical and health sciencesStructure-Activity RelationshipDrug StabilityDrug DiscoverymedicineGlucose homeostasisAnimalsHumansPPAR alphaReceptorCholesterol 7-alpha-HydroxylaseATP Binding Cassette Transporter Subfamily B Member 11chemistry.chemical_classificationBile acid010405 organic chemistryChemistryHEK 293 cellsImidazolesMembrane Transport ProteinsHep G2 Cells0104 chemical sciencesMolecular Docking SimulationZolpidem030104 developmental biologyHEK293 CellsBiochemistryMolecular MedicineFarnesoid X receptorATP-Binding Cassette TransportersSterol Regulatory Element Binding Protein 1HeLa CellsJournal of medicinal chemistry
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An Integrated Pharmacophore/Docking/3D-QSAR Approach to Screening a Large Library of Products in Search of Future Botulinum Neurotoxin A Inhibitors

2020

Botulinum toxins are neurotoxins produced by Clostridium botulinum. This toxin can be lethal for humans as a cause of botulism

0301 basic medicineModels MolecularBotulinum ToxinsDatabases FactualNeuromuscular transmissionQuantitative Structure-Activity RelationshipPharmacologymedicine.disease_cause01 natural sciencesType Alcsh:ChemistryModelsClostridium botulinumbotulinum neurotoxin ABotulismBotulinum Toxins Type Alcsh:QH301-705.5Spectroscopyfood and beveragesGeneral MedicineBotulinum neurotoxinComputer Science ApplicationsdockingPharmacophoreQuantitative structure–activity relationshipStatic ElectricityChemicalbotulinum neurotoxin A virtual screening docking 3D-QSAR molecular dynamicsMolecular Dynamics SimulationArticleCatalysisInorganic ChemistrySmall Molecule Libraries03 medical and health sciencesDatabasesmedicinePhysical and Theoretical ChemistryMolecular BiologyFactual3D-QSARVirtual screening010405 organic chemistrybusiness.industryfungiOrganic ChemistryMolecularHydrogen Bondingmedicine.diseasevirtual screeningmolecular dynamics0104 chemical sciences030104 developmental biologyModels Chemicallcsh:Biology (General)lcsh:QD1-999Docking (molecular)Clostridium botulinumbusinessInternational Journal of Molecular Sciences
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Rescuing the CFTR protein function: Introducing 1,3,4-oxadiazoles as translational readthrough inducing drugs.

2018

Nonsense mutations in the CFTR gene prematurely terminate translation of the CFTR mRNA leading to the production of a truncated protein that lacks normal function causing a more severe form of the cystic fibrosis (CF) disease. About 10% of patients affected by CF show a nonsense mutation. A potential treatment of this alteration is to promote translational readthrough of premature termination codons (PTCs) by Translational Readthrough Inducing Drugs (TRIDs) such as PTC124. In this context we aimed to compare the activity of PTC124 with analogues differing in the heteroatoms position in the central heterocyclic core. By a validated protocol consisting of computational screening, synthesis an…

0301 basic medicineModels MolecularCell SurvivalNonsense mutationCystic Fibrosis Transmembrane Conductance RegulatorSettore BIO/11 - Biologia MolecolareContext (language use)OxadiazoleSettore BIO/09 - FisiologiaCystic fibrosis03 medical and health sciencesStructure-Activity Relationship0302 clinical medicineDrug DiscoverymedicineHumansRNA MessengerGenetic disorderPharmacologyMessenger RNAOxadiazolesNonsense mutationDose-Response Relationship DrugMolecular StructureChemistryDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryTranslational readthroughPremature termination codonTranslation (biology)Settore CHIM/06 - Chimica OrganicaGeneral Medicinemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaSmall moleculeCell biologySettore BIO/18 - Genetica030104 developmental biologyBiological targetCystic fibrosi030220 oncology & carcinogenesisHeLa CellsEuropean journal of medicinal chemistry
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Addition of thiols to the double bond of dipeptide C-terminal dehydroalanine as a source of new inhibitors of cathepsin C.

2017

Addition of thiols to double bond of glycyl-dehydroalanine and phenyl-dehydroalanine esters provided micromolar inhibitors of cathepsin C. The structure-activity studies indicated that dipeptides containing N-terminal phenylalanine exhibit higher affinity towards the enzyme. A series of C-terminal S-substituted cysteines are responsible for varying interaction with S1 binding pocket of cathepsin C. Depending on diastereomer these compounds most likely act as slowly reacting substrates or competitive inhibitors. This was proved by TLC analysis of the medium in which interaction of methyl (S)-phenylalanyl-(R,S)-(S-adamantyl)cysteinate (7i) with the enzyme was studied. Molecular modeling enabl…

0301 basic medicineModels MolecularDouble bondStereochemistryPhenylalanineCysteine Proteinase InhibitorsBiochemistryCathepsin CCathepsin CSubstrate Specificity03 medical and health scienceschemistry.chemical_compoundStructure-Activity Relationship0302 clinical medicineDehydroalanineMoietyAnimalsSulfhydryl CompoundsBinding sitechemistry.chemical_classificationDipeptideAlanineBinding SitesDehydropeptidesDiastereomerEnzyme inhibitorsGeneral MedicineDipeptidesKinetics030104 developmental biologychemistryThiol addition030220 oncology & carcinogenesisCattleBiochimie
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Sensory domain contraction in histidine kinase CitA triggers transmembrane signaling in the membrane-bound sensor

2017

Bacteria use membrane-integral sensor histidine kinases (HK) to perceive stimuli and transduce signals from the environment to the cytosol. Information on how the signal is transmitted across the membrane by HKs is still scarce. Combining both liquid- and solid-state NMR, we demonstrate that structural rearrangements in the extracytoplasmic, citrate-sensing Per-Arnt-Sim (PAS) domain of HK CitA are identical for the isolated domain in solution and in a longer construct containing the membrane-embedded HK and lacking only the kinase core. We show that upon citrate binding, the PAS domain contracts, resulting in a shortening of the C-terminal β-strand. We demonstrate that this contraction of t…

0301 basic medicineModels MolecularHistidine Kinase030106 microbiologyMolecular ConformationCitric Acid03 medical and health sciencesStructure-Activity RelationshipBacterial ProteinsPAS domainProtein Interaction Domains and MotifsAmino Acid SequenceHistidineMultidisciplinaryChemistryKinaseHistidine kinaseGeobacillusMembrane ProteinsBiological SciencesTransmembrane proteinCell biologyCytosolHelixSignal transductionProtein BindingSignal Transduction
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Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer.

2016

Abstract As a master regulator of chromatin function, the lysine methyltransferase EZH2 orchestrates transcriptional silencing of developmental gene networks. Overexpression of EZH2 is commonly observed in human epithelial cancers, such as non–small cell lung carcinoma (NSCLC), yet definitive demonstration of malignant transformation by deregulated EZH2 remains elusive. Here, we demonstrate the causal role of EZH2 overexpression in NSCLC with new genetically engineered mouse models of lung adenocarcinoma. Deregulated EZH2 silences normal developmental pathways, leading to epigenetic transformation independent of canonical growth factor pathway activation. As such, tumors feature a transcrip…

0301 basic medicineModels MolecularLung Neoplasmsmedicine.medical_treatmentMolecular ConformationGene ExpressionAntineoplastic Agentsmacromolecular substancesBiologymedicine.disease_causeArticleMalignant transformationTargeted therapy03 medical and health sciencesMiceStructure-Activity RelationshipCell Line TumormedicineAnimalsHumansEnhancer of Zeste Homolog 2 ProteinMolecular Targeted TherapyLung cancerPromoter Regions GeneticGene Expression ProfilingEZH2Cancermedicine.diseaseMagnetic Resonance ImagingXenograft Model Antitumor AssaysChromatinrespiratory tract diseasesGene Expression Regulation NeoplasticDisease Models Animal030104 developmental biologyCell Transformation NeoplasticEnhancer Elements GeneticOncologyDrug DesignCancer researchAdenocarcinomaKRASEpigenetic therapyCancer discovery
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Identification of estrogen receptor α ligands with virtual screening techniques.

2016

Utilization of computer-aided molecular discovery methods in virtual screening (VS) is a cost-effective approach to identify novel bioactive small molecules. Unfortunately, no universal VS strategy can guarantee high hit rates for all biological targets, but each target requires distinct, fine-tuned solutions. Here, we have studied in retrospective manner the effectiveness and usefulness of common pharmacophore hypothesis, molecular docking and negative image-based screening as potential VS tools for a widely applied drug discovery target, estrogen receptor α (ERα). The comparison of the methods helps to demonstrate the differences in their ability to identify active molecules. For example,…

0301 basic medicineModels MolecularQuantitative structure–activity relationshipMolecular ConformationQuantitative Structure-Activity RelationshipComputational biologyMolecular Dynamics Simulationta3111BioinformaticsLigands01 natural sciencesMolecular Docking SimulationSmall Molecule Libraries03 medical and health sciencesestrogen receptor alphaDrug DiscoveryMaterials ChemistryHumansComputer SimulationPhysical and Theoretical ChemistrySpectroscopy3D-QSARVirtual screeningDrug discoveryChemistryta1182Estrogen Receptor alphaSmall Molecule LibrariesReproducibility of Resultsmolecular dockingvirtual screeningComputer Graphics and Computer-Aided DesignSmall molecule0104 chemical sciencesMolecular Docking Simulation010404 medicinal & biomolecular chemistry030104 developmental biologyArea Under Curvepharmacophore modelingligand discoverynegative imagePharmacophoreEstrogen receptor alphaJournal of molecular graphicsmodelling
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1,3,5-Triazines: A promising scaffold for anticancer drugs development

2017

This review covering literature reports from the beginning of this century to 2016 describes the synthetic pathways, the antitumor activity, the structure-activity relationship and, whenever reported, the possible mechanism of action of 1,3,5-triazine derivatives as well as of their hetero-fused compounds. Many 1,3,5-triazine derivatives, both uncondensed and hetero-fused, have shown remarkable antitumor activities and some of them reached clinical development.

0301 basic medicineModels MolecularScaffold31Disubstituted 135-triazineTrisubstituted 135-triazineAntineoplastic AgentsChemistry Techniques Synthetic01 natural sciences03 medical and health sciencesStructure-Activity RelationshipNeoplasmsDrug DiscoverymedicineAnimalsHumans5-TriazinesTrisubstituted 1Disubstituted 1Antitumor activityPharmacologyHeterofused 135-triazine010405 organic chemistryChemistryTriazinesNitrogen heterocyclesDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryGeneral MedicineHeterofused 1Combinatorial chemistry135-Triazine0104 chemical sciences030104 developmental biologyNitrogen heterocycleMechanism of action1; 3; 5-Triazines; Antitumor activity; Disubstituted 1; 3; 5-triazines; Heterofused 1; 3; 5-triazines; Nitrogen heterocycles; Trisubstituted 1; 3; 5-triazines; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Organic Chemistrymedicine.symptomAntitumor activity
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Investigation on Quantitative Structure-Activity Relationships of 1,3,4-Oxadiazole Derivatives as Potential Telomerase Inhibitors.

2020

Background:Telomerase, a reverse transcriptase, maintains telomere and chromosomes integrity of dividing cells, while it is inactivated in most somatic cells. In tumor cells, telomerase is highly activated, and works in order to maintain the length of telomeres causing immortality, hence it could be considered as a potential marker to tumorigenesis.A series of 1,3,4-oxadiazole derivatives showed significant broad-spectrum anticancer activity against different cell lines, and demonstrated telomerase inhibition.Methods:This series of 24 N-benzylidene-2-((5-(pyridine-4-yl)-1,3,4-oxadiazol-2yl)thio)acetohydrazide derivatives as telomerase inhibitors has been considered to carry out QSAR studies…

0301 basic medicineModels MolecularTelomeraseQuantitative structure–activity relationship2D descriptorsDatasets as TopicQuantitative Structure-Activity RelationshipAntineoplastic Agents010402 general chemistry01 natural sciencesModels BiologicalAnticancer activityMLR03 medical and health sciencesInhibitory Concentration 50Drug DiscoveryLeast-Squares AnalysisTelomerase134-oxadiazolesOxadiazolesMolecular StructureDrug discoveryChemistryQSARQuantitative structureCombinatorial chemistry0104 chemical sciencesTelomerase inhibitors030104 developmental biology1 3 4 oxadiazole derivativesDrug Screening Assays AntitumorCurrent drug discovery technologies
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In silico discovery of substituted pyrido[2,3-d]pyrimidines and pentamidine-like compounds with biological activity in myotonic dystrophy models

2016

Myotonic dystrophy type 1 (DM1) is a rare multisystemic disorder associated with an expansion of CUG repeats in mutant DMPK (dystrophia myotonica protein kinase) transcripts; the main effect of these expansions is the induction of pre-mRNA splicing defects by sequestering muscleblind-like family proteins (e.g. MBNL1). Disruption of the CUG repeats and the MBNL1 protein complex has been established as the best therapeutic approach for DM1, hence two main strategies have been proposed: targeted degradation of mutant DMPK transcripts and the development of CUG-binding molecules that prevent MBNL1 sequestration. Herein, suitable CUG-binding small molecules were selected using in silico approach…

0301 basic medicineMolecular biologyPhysiologyMutantMyotonic dystrophyDruggabilitylcsh:Medicine01 natural sciencesBiochemistryPhysical ChemistryMyoblastschemistry.chemical_compoundAnabolic AgentsMedicaments--InteraccióAnimal CellsDrug DiscoveryMedicine and Health SciencesMBNL1Drosophila ProteinsMyotonic Dystrophylcsh:ScienceRNA structureConnective Tissue CellsMultidisciplinaryMolecular StructureOrganic CompoundsStem CellsPhysicsRNA-Binding ProteinsBiological activityPhenotypeClimbingMolecular Docking SimulationNucleic acidsChemistryDrosophila melanogasterBiochemistryGenetic DiseasesConnective TissueRNA splicingPhysical SciencesCellular TypesAnatomyLocomotion57 - BiologiaSignal TransductionResearch ArticleBiotechnologyHydrogen bondingcongenital hereditary and neonatal diseases and abnormalitiesIn silicoPrimary Cell CultureComputational biologyBiology010402 general chemistryMyotonic dystrophyMyotonin-Protein KinaseDrug interactionsSmall Molecule Libraries03 medical and health sciencesStructure-Activity RelationshipmedicineAnimalsHumansRNA MessengerEnllaços d'hidrogenClinical GeneticsChemical PhysicsBiology and life sciencesChemical BondingBiological Locomotionlcsh:ROrganic ChemistryEstructura molecularChemical CompoundsHydrogen BondingCell BiologyFibroblastsmedicine.disease0104 chemical sciencesBenzamidinesAlternative SplicingDisease Models AnimalMacromolecular structure analysis030104 developmental biologyPyrimidinesBiological TissuechemistrySmall MoleculesRNAlcsh:QTrinucleotide Repeat ExpansionMolecular structure
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