Search results for "protein kinase inhibitors"

showing 10 items of 211 documents

Cardiotoxicity mechanisms of the combination of BRAF-inhibitors and MEK-inhibitors.

2018

Many new drugs have appeared in last years in the oncological treatment scenario. Each drug carries an important set of adverse events, not less, cardiovascular adverse events. This aspect is even more important considering the increasing use of combination therapies with two drugs, or three drugs as in some ongoing clinical trials. Besides it represents a growing problem for Cardiologists, that face it in every day clinical practice and that will face it probably more and more in the coming years. This work reviews the mechanism of action of BRAF-inhibitors and MEK-inhibitors used together, the pathophysiological mechanisms that lead to cardiovascular toxicity. Particularly, it focuses on …

DrugCardiovascular toxicityBRAF inhibitorProto-Oncogene Proteins B-rafmedicine.medical_specialtyCombination therapySettore MED/06 - Oncologia Medicamedia_common.quotation_subjectDecreased ejection fraction030204 cardiovascular system & hematologyCardiovascular System03 medical and health sciences0302 clinical medicineCardiovascular toxicityAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansPharmacology (medical)Intensive care medicineAdverse effectBRAF inhibitor; Cardio-oncology; Cardiovascular toxicity; Decreased ejection fraction; Hypertension; MEK inhibitor; Pharmacology; Pharmacology (medical)MelanomaProtein Kinase Inhibitorsmedia_commonPharmacologyMitogen-Activated Protein Kinase KinasesCardiotoxicityMEK inhibitorClinical Trials as Topicbusiness.industryMEK inhibitorCancermedicine.diseaseCardiotoxicityClinical trialCardio-oncology030220 oncology & carcinogenesisHypertensionbusinessPharmacologytherapeutics
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Intracellular retention of ABL kinase inhibitors determines commitment to apoptosis in CML cells

2012

PLoS one 7(7), e40853 (2012). doi:10.1371/journal.pone.0040853

Drugs and DevicesDrug Research and DevelopmentTime Factorsmedicine.drug_classChronic Myeloid LeukemiaIntracellular Spacelcsh:MedicineApoptosisPharmacologyPiperazinesTyrosine-kinase inhibitorHematologic Cancers and Related DisordersCell Line TumorLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesLeukemiasmedicineHumansAnnexin A5Proto-Oncogene Proteins c-abllcsh:ScienceProtein Kinase InhibitorsMyeloproliferative DisordersMultidisciplinaryABLDose-Response Relationship DrugCaspase 3Chemistrylcsh:RBiological activityImatinibHematologyrespiratory tract diseasesDasatinibKineticsPyrimidinesImatinib mesylatePharmacodynamicsBenzamidesImatinib MesylateMedicineATP-Binding Cassette Transporterslcsh:QDrug Screening Assays AntitumorSignal transductionIntracellularResearch ArticleSignal Transductionmedicine.drug
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Adverse events associated with encorafenib plus binimetinib in the COLUMBUS study: incidence, course and management.

2019

Abstract Background Dual inhibition of the mitogen-activated protein kinase pathway with BRAF/MEK inhibitor (BRAFi/MEKi) therapy is a standard treatment for BRAFV600-mutant metastatic melanoma and has historically been associated with grade III pyrexia or photosensitivity depending on the combination used. The objective of this study was to fully describe adverse events from the COLUMBUS study evaluating the most recent BRAF/MEK inhibitor combination encorafenib+binimetinib. Patients and methods Patients with locally advanced, unresectable or metastatic BRAFV600-mutant melanoma were randomised to receive encorafenib 450 mg once daily plus binimetinib 45 mg twice daily, encorafenib 300 mg on…

Encorafenib0301 basic medicineOncologyMaleCancer ResearchSkin NeoplasmsBinimetinib; Encorafenib; Melanoma; Safety; Vemurafenib;MedizinBinimetinibchemistry.chemical_compound0302 clinical medicineAntineoplastic Combined Chemotherapy Protocols1306 Cancer ResearchVemurafenibMelanomaFatigueeducation.field_of_studySulfonamidesMEK inhibitorMelanomaStandard treatmentIncidence10177 Dermatology ClinicBinimetinibNauseaMiddle AgedOncology030220 oncology & carcinogenesis2730 OncologyFemaleSafetyMitogen-Activated Protein Kinasesmedicine.drugProto-Oncogene Proteins B-rafmedicine.medical_specialtyVomitingPopulation610 Medicine & health03 medical and health sciencesInternal medicinemedicineHumanseducationAdverse effectProtein Kinase Inhibitorsbusiness.industrymedicine.diseaseDiscontinuation030104 developmental biologychemistryVemurafenibMutationBenzimidazolesCarbamatesbusinessEuropean journal of cancer (Oxford, England : 1990)
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The Co‐mutational Spectrum Determines the Therapeutic Response in Murine FGFR2 Fusion‐Driven Cholangiocarcinoma

2021

Background and aims Intrahepatic cholangiocarcinoma (ICC) is the second most common primary liver cancer and a highly lethal malignancy. Chemotherapeutic options are limited, but a considerable subset of patients harbors genetic lesions for which targeted agents exist. Fibroblast growth factor receptor 2 (FGFR2) fusions belong to the most frequent and therapeutically relevant alterations in ICC, and the first FGFR inhibitor was recently approved for the treatment of patients with progressed, fusion-positive ICC. Response rates of up to 35% indicate that FGFR-targeted therapies are beneficial in many but not all patients. Thus far, no established biomarkers exist that predict resistance or r…

Fetal Proteins0301 basic medicineAntimetabolites AntineoplasticCombination therapymedicine.medical_treatmentFGFR InhibitionVesicular Transport ProteinsCyclic AMP Response Element-Binding Protein Amedicine.disease_causeDeoxycytidineMalignant transformationTargeted therapyCholangiocarcinomaProto-Oncogene Proteins p21(ras)Mice03 medical and health sciencesLiver Neoplasms Experimental0302 clinical medicineAntigens NeoplasmmedicineAnimalsReceptor Fibroblast Growth Factor Type 2Protein Kinase InhibitorsCell ProliferationHepatologyOncogenebusiness.industryFibroblast growth factor receptor 2AdenosylhomocysteinasePhenylurea CompoundsGemcitabineBile Ducts IntrahepaticCell Transformation NeoplasticPyrimidines030104 developmental biologyBile Duct NeoplasmsFibroblast growth factor receptorMutationCancer research030211 gastroenterology & hepatologyKRASGene FusionbusinessCo-Repressor ProteinsMicrotubule-Associated ProteinsHepatology
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Design of antitumor drugs targeting c-kit receptor by a new mixed ligand-structure based method

2020

An important challenge, in the medicinal chemistry field, is the research of novel forceful drugs to overcome tumor-acquired resistance. The c-Kit tyrosine kinase receptor (TKR) represents a suitable target for the carcinogenesis control of gastro-intestinal stromal (GIST), leukemia, and mastocytosis tumors; nevertheless, several hotspot mutations of the protein limit the efficacy of a few clinical administered TKRs inhibitors. In this study, a new in silico protocol based on ligand and structure-based combined method is proposed, with the aim to identify a set of new c-Kit inhibitors able to complex c-Kit mutated proteins. A recent and freely available web-server DRUDIT is used for the lig…

Gastrointestinal Stromal TumorsIn silicoAntineoplastic AgentsComputational biologyDrug resistanceIn silico protocolsmedicine.disease_causeLigandsReceptor tyrosine kinase03 medical and health sciences0302 clinical medicineDRUDIT web-serverc-KitMaterials ChemistrymedicineHumansPhysical and Theoretical ChemistryProtein Kinase InhibitorsSpectroscopy030304 developmental biology0303 health sciencesbiologyChemistryLigandMixed ligandmedicine.diseaseComputer Graphics and Computer-Aided DesignLeukemiaProto-Oncogene Proteins c-kitDocking (molecular)Drug Resistance Neoplasm030220 oncology & carcinogenesisDrug resistanceMutationMolecular dockingbiology.proteinCarcinogenesis
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Targeting the JAK/STAT Pathway: A Combined Ligand- and Target-Based Approach

2021

Janus kinases (JAKs) are a family of proinflammatory enzymes able to mediate the immune responses and the inflammatory cascade by modulating multiple cytokine expressions as well as various growth factors. In the present study, the inhibition of the JAK-signal transducer and activator of transcription (STAT) signaling pathway is explored as a potential strategy for treating autoimmune and inflammatory disorders. A computationally driven approach aimed at identifying novel JAK inhibitors based on molecular topology, docking, and molecular dynamics simulations was carried out. For the best candidates selected, the inhibitory activity against JAK2 was evaluated in vitro. Two hit compounds with…

General Chemical EngineeringTransducersBioinformatics and computational biology Inhibitors Inhibition Peptides and proteins MoleculesLibrary and Information SciencesLigands01 natural sciencesstatArticleProinflammatory cytokine0103 physical sciencesProtein Kinase InhibitorsJanus KinasesTofacitinib010304 chemical physicsActivator (genetics)ChemistryJAK-STAT signaling pathwayGeneral Chemistry0104 chemical sciencesComputer Science ApplicationsCell biology010404 medicinal & biomolecular chemistryDocking (molecular)Signal transductionJanus kinaseSignal TransductionJournal of Chemical Information and Modeling
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Design, Synthesis and Biological Evaluation of 7-Chloro-9

2019

Glycogen synthase kinase-3β (GSK-3β) represents a relevant drug target for the treatment of neurodegenerative pathologies including Alzheimer’s disease. We herein report on the optimization of a novel class of GSK-3β inhibitors based on the tofacitinib-derived screen hit 3-((3R,4R)-3-((7-chloro-9H-pyrimido[4,5-b]indol-4-yl)(methyl)amino)-4-methylpiperidin-1-yl)-3-oxopropanenitrile (1). We synthesized a series of 19 novel 7-chloro-9H-pyrimido[4,5-b]indole-based derivatives and studied their structure–activity relationships with focus on the cyanoacetyl piperidine moiety. We unveiled the crucial role of the nitrile group and its importance for the activity of this compound series. A successfu…

Glycogen synthase kinase-3βBinding SitesGlycogen Synthase Kinase 3 betatofacitinibDose-Response Relationship DrugMolecular Structurekinase inhibitorMolecular Conformationprotein kinaseChemistry Techniques SyntheticMolecular Dynamics SimulationArticle7-chloro-9H-pyrimido[45-b]indoleEnzyme ActivationMolecular Docking SimulationStructure-Activity RelationshipAdenosine TriphosphateDrug DesignHumansEnzyme InhibitorsHydrophobic and Hydrophilic InteractionsProtein Kinase InhibitorsProtein BindingMolecules (Basel, Switzerland)
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H89 enhances the sensitivity of cancer cells to glyceryl trinitrate through a purinergic receptor-dependent pathway

2014

// Marion Cortier 1, 2, 3 , Rahamata Boina-Ali 1, 2, 3 , Cindy Racoeur 1, 2, 3 , Catherine Paul 1, 2, 3 , Eric Solary 2, 4, 5 , Jean-Francois Jeannin 1, 2, 3 , Ali Bettaieb 1, 2, 3 1 EPHE, Tumor Immunology and Immunotherapy Laboratory, Dijon, F-21000, France 2 Inserm U866, Dijon, F-21000, France 3 EA7269, University of Burgundy, Dijon, F-21000, France 4 Inserm UMR1009, Gustave Roussy Institute, Villejuif F-94805, France 5 University Paris-Sud, Faculty of Medicine, Le Kremlin-Bicetre, F-94800, France Correspondence to: Ali Bettaieb, e-mail: ali.bettaieb@u-bourgogne.fr Keywords: H89, GTN, cancer, purinergic receptors, cGMP Received: October 08, 2014      Accepted: January 09, 2015      Publis…

H89SuraminApoptosisPharmacologyBiologyNitric OxideTransfectionNitric oxideMiceNitroglycerinReceptors Purinergic P2Y1chemistry.chemical_compoundAdenosine TriphosphateCell Line TumorNeoplasmspurinergic receptorsmedicineAnimalsHumanscancerCytotoxic T cellReceptorProtein Kinase InhibitorsMembrane Potential MitochondrialSulfonamidesReceptors Purinergic P2Gene Expression ProfilingPurinergic receptorReceptors PurinergicDrug SynergismOligonucleotides AntisenseIsoquinolinescGMPOncologychemistryApoptosisColonic NeoplasmsCancer cellcardiovascular systemSignal transductionReactive Oxygen SpeciesGTNReceptors Purinergic P2X3circulatory and respiratory physiologySignal TransductionResearch Papermedicine.drugOncotarget
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Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain.

2005

Activating mutations in the FLT3 tyrosine kinase (TK) occur in approximately 35% of patients with acute myeloid leukemia (AML). Therefore, targeting mutated FLT3 is an attractive therapeutic strategy, and early clinical trials testing FLT3 TK inhibitors (TKI) showed measurable clinical responses. Most of these responses were transient; however, in a subset of patients blast recurrence was preceded by an interval of prolonged remission. The etiology of clinical resistance to FLT3-TKI in AML is unclear but is of major significance for the development of future therapeutic strategies. We searched for mechanisms of resistance in 6 patients with AML who had relapses upon PKC412 treatment. In an …

ImmunologyMutation MissenseBiologyBiochemistrychemistry.chemical_compoundIn vivoRecurrencehemic and lymphatic diseasesHumansProtein Kinase InhibitorsProtein Kinase CQuizartinibKinaseMyeloid leukemiaCell BiologyHematologyProtein-Tyrosine KinasesStaurosporineEnzyme ActivationProtein kinase domainchemistryfms-Like Tyrosine Kinase 3Drug Resistance NeoplasmLeukemia MyeloidFms-Like Tyrosine Kinase 3Acute DiseaseCancer researchTyrosine kinaseCrenolanibBlood
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Design and synthesis of 1-aryl-5-anilinoindazoles as c-Jun N-terminal kinase inhibitors.

2012

Starting from pyrazole HTS hit (1), a series of 1-aryl-1H-indazoles have been synthesized as JNK3 inhibitors with moderate selectivity against JNK1. SAR studies led to the synthesis of 5r as double digital nanomolar JNK3 inhibitor with good in vivo exposure.

IndazolesStereochemistryClinical BiochemistryPharmaceutical SciencePlasma protein bindingPyrazoleBiochemistrychemistry.chemical_compoundStructure-Activity RelationshipIn vivoMitogen-Activated Protein Kinase 10Drug DiscoveryStructure–activity relationshipAnimalsMitogen-Activated Protein Kinase 8Molecular BiologyProtein Kinase InhibitorsAniline CompoundsChemistryKinaseArylOrganic Chemistryc-junJNK Mitogen-Activated Protein KinasesBrainCombinatorial chemistryRatsDrug DesignMolecular MedicineSelectivityHalf-LifeProtein BindingBioorganicmedicinal chemistry letters
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