Search results for "Azoles"

showing 10 items of 899 documents

2 H-1,2,3-Triazole-Based Dipeptidyl Nitriles: Potent, Selective, and Trypanocidal Rhodesain Inhibitors by Structure-Based Design.

2018

Macrocyclic inhibitors of rhodesain (RD), a parasitic cysteine protease and drug target for the treatment of human African trypanosomiasis, have shown low metabolic stability at the macrocyclic ether bridge. A series of acyclic dipeptidyl nitriles was developed using structure-based design (PDB ID: 6EX8). The selectivity against the closely related cysteine protease human cathepsin L (hCatL) was substantially improved, up to 507-fold. In the S2 pocket, 3,4-dichlorophenylalanine residues provided high trypanocidal activities. In the S3 pocket, aromatic residues provided enhanced selectivity against hCatL. RD inhibition (Ki values) and in vitro cell-growth of Trypanosoma brucei rhodesiense (I…

0301 basic medicineTrypanosoma brucei rhodesienseStereochemistrySwineTrypanosoma cruziPlasmodium falciparumTriazoleProtozoan ProteinsCysteine Proteinase InhibitorsLigands01 natural sciencesCysteine Proteinase InhibitorsCell LineCathepsin L03 medical and health scienceschemistry.chemical_compoundMiceStructure-Activity RelationshipIn vivoDrug DiscoveryNitrilesStructure–activity relationshipAnimalsHumansATP Binding Cassette Transporter Subfamily B Member 1Trypanocidal agentBinding SitesbiologyMolecular Structure010405 organic chemistryChemistryTrypanosoma brucei rhodesienseDipeptidesTriazolesCysteine proteaseTrypanocidal Agents0104 chemical sciencesRatsCysteine Endopeptidases030104 developmental biologyDrug Designbiology.proteinMicrosomes LiverMolecular MedicineFemaleLeishmania donovaniJournal of medicinal chemistry
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Simple dialkyl pyrazole-3,5-dicarboxylates show in vitro and in vivo activity against disease-causing trypanosomatids.

2017

SUMMARYThe synthesis and antiprotozoal activity of some simple dialkyl pyrazole-3,5-dicarboxylates (compounds 2–6) and their sodium salts (pyrazolates) (compounds 7–9) against Trypanosoma cruzi, Leishmania infantum and Leishmania braziliensis are reported. In most cases the studied compounds showed, especially against the clinically significant amastigote forms, in vitro activities higher than those of the reference drugs (benznidazole for T. cruzi and glucantime for Leishmania spp.); furthermore, the low non-specific cytotoxicities against Vero cells and macrophages shown by these compounds led to good selectivity indexes, which are 8–72 times higher for T. cruzi amastigotes and 15–113 tim…

0301 basic medicineTrypanosomamedicine.drug_classTrypanosoma cruziParasitemiaLeishmania braziliensisMicrobiology03 medical and health sciencesMiceIn vivoChlorocebus aethiopsparasitic diseasesmedicineAnimalsChagas DiseaseDicarboxylic AcidsLeishmania infantumAmastigoteTrypanosoma cruziVero CellsLeishmaniaMice Inbred BALB CbiologyMacrophagesbiology.organism_classificationLeishmaniaLeishmania braziliensisTrypanocidal Agentsantichagasic activitypyrazole030104 developmental biologyInfectious DiseasesBenznidazoleleishmanicidal activityAntiprotozoalcytotoxicityPyrazolesAnimal Science and ZoologyParasitologyFemaleLeishmania infantummedicine.drug
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Targeting Nonsense: Optimization of 1,2,4-Oxadiazole TRIDs to Rescue CFTR Expression and Functionality in Cystic Fibrosis Cell Model Systems

2020

Cystic fibrosis (CF) patients develop a severe form of the disease when the cystic fibrosis transmembrane conductance regulator (CFTR) gene is affected by nonsense mutations. Nonsense mutations are responsible for the presence of a premature termination codon (PTC) in the mRNA, creating a lack of functional protein. In this context, translational readthrough-inducing drugs (TRIDs) represent a promising approach to correct the basic defect caused by PTCs. By using computational optimization and biological screening, we identified three new small molecules showing high readthrough activity. The activity of these compounds has been verified by evaluating CFTR expression and functionality after…

0301 basic medicineYellow fluorescent proteinCystic Fibrosisnonsense mutationCystic Fibrosis Transmembrane Conductance RegulatorCystic fibrosislcsh:Chemistry0302 clinical medicinelcsh:QH301-705.5SpectroscopyCells CulturedbiologyChemistryGeneral MedicineSmall moleculeCystic fibrosis transmembrane conductance regulatorComputer Science ApplicationsCell biologyCodon Nonsense030220 oncology & carcinogenesisNonsense mutationContext (language use)Settore BIO/11 - Biologia MolecolareCatalysisArticleInorganic Chemistry03 medical and health sciencesmedicineHumansRNA MessengerPhysical and Theoretical ChemistryMolecular BiologyGeneMessenger RNAOrganic ChemistryoxadiazolesSettore CHIM/06 - Chimica Organicapremature termination codonmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulationlcsh:Biology (General)lcsh:QD1-999translational readthrough inducing drugsProtein BiosynthesisMutationbiology.proteingenetic disorderInternational Journal of Molecular Sciences
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Anticancer properties of 5Z-(4- fuorobenzylidene)-2-(4- hydroxyphenylamino)-thiazol-4-one

2019

Abstract4-thiazolidinones, which are privileged structures in medicinal chemistry, comprise the well-known class of heterocycles and are a source of new drug-like compounds. Undoubtedly, the 5-bulky-substituted-2,4-thiazolidinediones - a class of antihyperglycemic glitazones, which are peroxisome proliferator-activated receptor gamma (PPARγ) agonists, are the most described group among them. As there are various chemically distinct 4-thiazolidinones, different subtypes have been selected for studies; however, their main pharmacological profiles are similar. The aim of this study was to evaluate the anticancer activity of 5Z-(4-fluorobenzylidene)-2-(4-hydroxyphenylamino)-thiazol-4-one (Les-2…

0301 basic medicinelcsh:MedicineAntineoplastic AgentsApoptosisDrug developmentArticle03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorLactate dehydrogenaseHumansViability assaylcsh:ScienceCytotoxicityReceptorchemistry.chemical_classificationReactive oxygen speciesMultidisciplinaryDose-Response Relationship DrugL-Lactate DehydrogenaseMolecular medicineCaspase 3lcsh:RMetabolismPeroxisomeThiazoles030104 developmental biologychemistryBiochemistryA549 CellsPreclinical researchCell culturelcsh:QCaco-2 CellsReactive Oxygen Species030217 neurology & neurosurgeryScientific Reports
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Strategies against nonsense: oxadiazoles as translational readthrough-inducing drugs (TRIDs)

2019

This review focuses on the use of oxadiazoles as translational readthrough-inducing drugs (TRIDs) to rescue the functional full-length protein expression in mendelian genetic diseases caused by nonsense mutations. These mutations in specific genes generate premature termination codons (PTCs) responsible for the translation of truncated proteins. After a brief introduction on nonsense mutations and their pathological effects, the features of various classes of TRIDs will be described discussing differences or similarities in their mechanisms of action. Strategies to correct the PTCs will be presented, particularly focusing on a new class of Ataluren-like oxadiazole derivatives in comparison …

0301 basic medicinemedia_common.quotation_subjectNonsenseNonsense mutationRegulatorSettore BIO/11 - Biologia MolecolareReviewComputational biologyBiologyOxadiazoleCatalysiscystic fibrosislcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicineAtalurenTranslational readthrough inducing drugsPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyGeneSpectroscopymedia_commonNonsense mutationOrganic ChemistryTranslational readthroughoxadiazolesPremature termination codonTranslation (biology)General MedicineSettore CHIM/06 - Chimica OrganicaSmall moleculeSettore CHIM/08 - Chimica FarmaceuticaTransmembrane proteinComputer Science ApplicationsSettore BIO/18 - Genetica030104 developmental biologyPharmaceutical Preparationslcsh:Biology (General)lcsh:QD1-999Codon NonsenseProtein Biosynthesis030220 oncology & carcinogenesisCystic fibrosi
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Genotoxicity and Epigenotoxicity of Carbazole-Derived Molecules on MCF-7 Breast Cancer Cells

2021

The carbazole compounds PK9320 (1-(9-ethyl-7-(furan-2-yl)-9H-carbazol-3-yl)-N-methylmethanamine) and PK9323 (1-(9-ethyl-7-(thiazol-4-yl)-9H-carbazol-3-yl)-N-methylmethanamine), second-generation analogues of PK083 (1-(9-ethyl-9H-carbazol-3-yl)-N-methylmethanamine), restore p53 signaling in Y220C p53-mutated cancer cells by binding to a mutation-induced surface crevice and acting as molecular chaperones. In the present paper, these three molecules have been tested for mutant p53-independent genotoxic and epigenomic effects on wild-type p53 MCF-7 breast adenocarcinoma cells, employing a combination of Western blot for phospho-γH2AX histone, Comet assay and methylation-sensitive arbitrarily pr…

0301 basic medicinemedicine.disease_causeEpigenesis GeneticHistoneslcsh:Chemistry0302 clinical medicineSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopyEpigenomicsDNA methylationbiologyChemistryGeneral Medicine3. Good healthComputer Science Applicationscarbazole derivativeHistone030220 oncology & carcinogenesisDNA methylationMCF-7 CellsFemaleepigeneticSignal TransductionCarbazolesAntineoplastic AgentsBreast NeoplasmsArticleCatalysisInorganic Chemistry03 medical and health sciencesbreast cancermedicineHumansEpigeneticsPhysical and Theoretical ChemistryMolecular BiologyepigeneticsOrganic Chemistrygenomic instabilityComet assaySettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999MCF-7carbazole derivativesCancer cellbiology.proteinCancer researchTumor Suppressor Protein p53GenotoxicityDNA DamageMutagensInternational Journal of Molecular Sciences
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CHK1-targeted therapy to deplete DNA replication-stressed, p53-deficient, hyperdiploid colorectal cancer stem cells.

2017

ObjectiveCancer stem cells (CSCs) are responsible for tumour formation and spreading, and their targeting is required for tumour eradication. There are limited therapeutic options for advanced colorectal cancer (CRC), particularly for tumours carrying RAS-activating mutations. The aim of this study was to identify novel CSC-targeting strategies.DesignTo discover potential therapeutics to be clinically investigated as single agent, we performed a screening with a panel of FDA-approved or investigational drugs on primary CRC cells enriched for CSCs (CRC-SCs) isolated from 27 patients. Candidate predictive biomarkers of efficacy were identified by integrating genomic, reverse-phase protein mic…

0301 basic medicinep53DNA ReplicationCELL CYCLE CONTROLDNA damageColorectal cancerColonmedicine.medical_treatmentAntineoplastic AgentsBiologyBioinformaticsmedicine.disease_causeDNA DAMAGETargeted therapy03 medical and health sciencesCancer stem cellCell Line TumormedicineHumansCHEK11506DRUG DEVELOPMENTOligonucleotide Array Sequence AnalysisMutationCOLORECTAL CANCERSettore MED/06 - ONCOLOGIA MEDICAGastroenterologyCHEMOTHERAPYmedicine.diseaseImmunohistochemistryPrexasertib030104 developmental biologyPyrazinesCheckpoint Kinase 1MutationCancer researchNeoplastic Stem CellsPyrazolesStem cellTumor Suppressor Protein p53Colorectal NeoplasmsGut
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Ataluren for the Treatment of Usher Syndrome 2A Caused by Nonsense Mutations

2019

The identification of genetic defects that underlie inherited retinal diseases (IRDs) paves the way for the development of therapeutic strategies. Nonsense mutations caused approximately 12% of all IRD cases, resulting in a premature termination codon (PTC). Therefore, an approach that targets nonsense mutations could be a promising pharmacogenetic strategy for the treatment of IRDs. Small molecules (translational read-through inducing drugs

0301 basic medicinepatient-derived fibroblastsUsher syndromechemistry.chemical_compound0302 clinical medicineMedicineTRIDSpectroscopyCells CulturedExtracellular Matrix ProteinsOxadiazolesGeneral MedicinePhenotypeImmunohistochemistryComputer Science ApplicationsRetinitis pigmentosaCodon Nonsenseocular therapyUsher syndromeUsher SyndromesNonsense mutationModels BiologicalCatalysisArticleInorganic Chemistry03 medical and health sciencesStructure-Activity RelationshipAtalurenCiliogenesisparasitic diseasesRetinitis pigmentosaHumansGenetic Predisposition to DiseasePhysical and Theoretical ChemistryMolecular BiologyGenetranslational read-throughbusiness.industryOrganic ChemistryHEK 293 cellsFibroblastsmedicine.diseaseAtaluren030104 developmental biologyHEK293 CellschemistryProtein BiosynthesisMutationCancer researchbusiness030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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Development of a method to determine axitinib, lapatinib and afatinib in plasma by micellar liquid chromatography and validation by the European Medi…

2017

A method based on micellar liquid chromatography to quantify the tyrosine kinase inhibitors axitinib, lapatinib and afatinib in plasma is reported. The sample pretreatment was a simple 1/5-dilution in a pure micellar solution, filtration and direct injection, without requiring extraction or purification steps. The three drugs were resolved from the matrix in 17 min, using an aqueous solution of 0.07 M sodium dodecyl sulfate – 6.0% 1-pentanol, buffered at pH 7 with 0.01 M phosphate salt as mobile phase, running under isocratic mode at 1 mL/min through a C18 column. The detection was performed by absorbance at 260 nm. An accurate mathematical relationship was established between the retention…

0301 basic medicineretentionBioanalysisIndazolesAxitinibbioanalysisClinical BiochemistryAntineoplastic AgentsAfatinib01 natural sciencesBiochemistryMicelleAnalytical ChemistryMatrix (chemical analysis)03 medical and health scienceschemistry.chemical_compoundDrug StabilityPulmonary surfactantLimit of DetectionNeoplasmsdirect injectionHumansSodium dodecyl sulfateMicellesDetection limitAqueous solutionChromatographyChemistry010401 analytical chemistryImidazolesReproducibility of ResultsmodelingLapatinibCell BiologyGeneral Medicine0104 chemical sciences030104 developmental biologyanti-cancer drugMicellar liquid chromatographyLinear ModelsQuinazolinesoptimizationChromatography LiquidJournal of Chromatography B
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New Thiazole Nortopsentin Analogues Inhibit Bacterial Biofilm Formation.

2018

New thiazole nortopsentin analogues were conveniently synthesized and evaluated for their activity as inhibitors of biofilm formation of relevant Gram-positive and Gram-negative pathogens. All compounds were able to interfere with the first step of biofilm formation in a dose-dependent manner, showing a selectivity against the staphylococcal strains. The most active derivatives elicited IC50 values against Staphylococcus aureus ATCC 25923, ranging from 0.40&ndash

0301 basic medicinethiazole derivativeAquatic OrganismsIndolesDrug ResistancePharmaceutical ScienceBacterial growthAntibiofilm agentmedicine.disease_cause01 natural scienceschemistry.chemical_compoundDrug Discoveryanti-virulence agents; antibiofilm agents; marine alkaloids; nortopsentin analogues; thiazole derivatives; Anti-Bacterial Agents; Aquatic Organisms; Biofilms; Humans; Imidazoles; Indoles; Inhibitory Concentration 50; Staphylococcal Infections; Staphylococcus aureus; Thiazoles; Drug Resistance; Bacterial; Anti-virulence agents; Antibiofilm agents; Marine alkaloids; Nortopsentin analogues; Thiazole derivativesPharmacology Toxicology and Pharmaceutics (miscellaneous)lcsh:QH301-705.5Aquatic OrganismBiofilmBacterialImidazolesantibiofilm agentsStaphylococcal InfectionsAnti-Bacterial Agentsnortopsentin analoguesBiochemistryStaphylococcus aureusStaphylococcus aureumarine alkaloidsthiazole derivativesSelectivityHumanStaphylococcus aureusAnti-virulence agentNortopsentin analogueArticle03 medical and health sciencesInhibitory Concentration 50Anti-Bacterial AgentDrug Resistance BacterialIc50 valuesmedicineHumansThiazoleImidazoleStaphylococcal Infection010405 organic chemistryBiofilmSettore CHIM/08 - Chimica Farmaceutica0104 chemical sciencesmarine alkaloidThiazoles030104 developmental biologychemistrylcsh:Biology (General)anti-virulence agentsIndoleBiofilmsThiazoleMarine drugs
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