Search results for "protein kinase inhibitors"

showing 10 items of 211 documents

Synthesis and Antitumor Activity of 3-(2-Phenyl-1,3-thiazol-4-yl)-1H-indoles and 3-(2-Phenyl-1,3-thiazol-4-yl)-1H-7-azaindoles

2011

Given the potent antimicrobial, antiviral, and antitumor activities of many natural products, there is an increasing interest in the synthesis of new molecules based on natural compound scaffolds. Based on a 2,4-bis(3'-indolyl)imidazole skeleton, two new series of phenylthiazolylindoles and phenylthiazolyl-7-azaindoles were obtained by Hantzsch reaction between substituted phenylthioamides and the α-bromoacetyl derivatives. Some azaindole derivatives, tested at the National Cancer Institute against a panel of ∼60 tumor cell lines derived from nine human cancer cell types, showed inhibitory effects against all cell lines investigated at micromolar to nanomolar concentrations. Two of them exh…

IndolesStereochemistry3-(2-Phenyl-1; 3-thiazol-4-yl)-1H-indoles; 3-(2-Phenyl-1; 3-thiazol-4-yl)-1H-7-azaindoles; Nortopsentins; Antitumor activityAntineoplastic AgentsTumor cells3-thiazol-4-yl)-1H-7-azaindolesBiochemistry3-(2-Phenyl-13-thiazol-4-yl)-1H-indolechemistry.chemical_compoundCell Line TumorNeoplasmsCDC2 Protein KinaseDrug DiscoveryHumansImidazoleGeneral Pharmacology Toxicology and PharmaceuticsProtein Kinase InhibitorsPharmacologyAntitumor activityNortopsentins3-thiazol-4-yl)-1H-indolesChemistryKinaseNatural compoundNortopsentinOrganic Chemistry3-(2-Phenyl-1AntimicrobialCombinatorial chemistryThiazolesCell culture3-(2-Phenyl-13-thiazol-4-yl)-1H-7-azaindoleMolecular MedicineDrug Screening Assays AntitumorAntitumor activityHuman cancer
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A New Oxadiazole-Based Topsentin Derivative Modulates Cyclin-Dependent Kinase 1 Expression and Exerts Cytotoxic Effects on Pancreatic Cancer Cells

2021

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal form of cancer characterized by drug resistance, urging new therapeutic strategies. In recent years, protein kinases have emerged as promising pharmacological targets for the treatment of several solid and hematological tumors. Interestingly, cyclin-dependent kinase 1 (CDK1) is overexpressed in PDAC tissues and has been correlated to the aggressive nature of these tumors because of its key role in cell cycle progression and resistance to the induction of apoptosis. For these reasons, CDK1 is one of the main causes of chemoresistance, representing a promising pharmacological target. In this study, we report the synthesis of new 1,2,4…

Indolespancreatic cancerPharmaceutical ScienceAntineoplastic AgentsApoptosisArticleAnalytical ChemistryStructure-Activity RelationshipQD241-441CDK1 inhibitorantiproliferativeCatalytic DomainCell Line TumorDrug DiscoveryCDC2 Protein KinaseHumansPhysical and Theoretical ChemistryProtein Kinase InhibitorsCell ProliferationOxadiazolesOrganic ChemistryImidazoles124-oxadiazolePDACmarine alkaloidMolecular Docking SimulationPancreatic NeoplasmsChemistry (miscellaneous)Molecular Medicinemarine alkaloidstopsentinDrug Screening Assays Antitumor124-oxadiazole; marine alkaloids; topsentin; CDK1 inhibitor; pancreatic cancer; PDAC; antiproliferative; apoptosisCarcinoma Pancreatic DuctalProtein BindingSignal TransductionMolecules
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Structure–activity relationships, and drug metabolism and pharmacokinetic properties for indazole piperazine and indazole piperidine inhibitors of RO…

2007

ROCK has been implicated in many diseases ranging from glaucoma to spinal cord injury and is therefore an important target for therapeutic intervention. In this study, we have designed a series of 1-(4-(1H-indazol-5-yl)piperazin-1-yl)-2-hydroxy(or 2-amino) analogs and a series of 1-(4-(1H-indazol-5-yl amino)piperidin-1-yl)-2-hydroxy(or 2-amino) inhibitors of ROCK-II. SR-1459 has IC50 = 13 nM versus ROCK-II while the IC50s for SR-715 and SR-899 are 80 nM and 100 nM, respectively. Many of these inhibitors, especially the 2-amino substituted analogs for both series, are modest/potent CYP3A4 inhibitors as well. However, a few of these inhibitors (SR-715 and SR-899) show strong selectivity for R…

KinaseIndazolesInhibitorStereochemistryClinical BiochemistryPharmaceutical ScienceProtein Serine-Threonine KinasesPharmacologyBiochemistryPiperazinesInhibitory Concentration 50Structure-Activity Relationshipchemistry.chemical_compoundDrug StabilityPiperidinesIn vivoDrug DiscoveryAnimalsCytochrome P-450 CYP3ACytochrome P-450 Enzyme InhibitorsHumansStructure–activity relationshipPharmacokineticsRho-kinaseProtein Kinase InhibitorsMolecular BiologyCytochrome P-450 Enzyme Inhibitorsrho-Associated KinasesIndazoleCYP3A4Organic ChemistryIntracellular Signaling Peptides and ProteinsROCK-IIRatsPiperazinePharmaceutical PreparationschemistryMolecular MedicinePiperidineDrug metabolismBioorganic & Medicinal Chemistry Letters : a tetrahedron publication for the rapid dissemination of preliminary communication and all aspects of bioorganic chemistry, medicinal chemistry and related disciplines
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Severe metabolic alterations in liver cancer lead to ERK pathway activation and drug resistance

2020

Background: The extracellular signal-regulated kinase (ERK) pathway regulates cell growth, and is hyper-activated and associated with drug resistance in hepatocellular carcinoma (HCC). Metabolic pathways are profoundly dysregulated in HCC. Whether an altered metabolic state is linked to activated ERK pathway and drug response in HCC is unaddressed. Methods: We deprived HCC cells of glutamine to induce metabolic alterations and performed various assays, including metabolomics (with 13C-glucose isotope tracing), microarray analysis, and cell proliferation assays. Glutamine-deprived cells were also treated with kinase inhibitors (e.g. Sorafenib, Erlotinib, U0126 amongst other MEK inhibitors). …

Life sciences; biology0301 basic medicineSorafenibMAPK/ERK pathwayCarcinoma HepatocellularResearch paperMAP Kinase Signaling SystemGlutamineProliferationlcsh:MedicineAntineoplastic AgentsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineDownregulation and upregulationddc:570medicineSerineHumansHCCProtein Kinase InhibitorsCell Proliferationlcsh:R5-920Cell growthChemistryKinaseMicroarray analysis techniquesLiver Neoplasmslcsh:RGeneral MedicineHep G2 Cellsdigestive system diseasesMetabolic pathway030104 developmental biologyAnaerobic glycolysisDrug Resistance NeoplasmKinase inhibitors030220 oncology & carcinogenesisCancer researchMetabolomeMetabolic stateAerobic glycolysisTranscriptomelcsh:Medicine (General)medicine.drugEBioMedicine
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The antifibrotic potential of a sustained release formulation of a PDGF beta-receptor targeted rho kinase inhibitor

2019

Rho kinase activity in hepatic stellate cells (HSCs) is associated with activation, transformation and contraction of these cells, leading to extracellular matrix production and portal hypertension in liver cirrhosis. Inhibition of rho kinase activity can reduce these activities, but may also lead to side effects, for instance systemic hypotension. This can be circumvented by liver-specific delivery of a rho kinase inhibitor to effector cells. Therefore, we targeted the rho kinase inhibitor Y27632 to the key pathogenic cells in liver fibrosis, i.e. myofibroblasts including activated HSCs that highly express the PDGF beta-receptor, using the drug carrier pPB-MSA. This carrier consists of mou…

Liver CirrhosisDrug targetingPyridinesPolymeric microspheresPharmaceutical Science02 engineering and technologyPharmacologychemistry.chemical_compoundY-27632FibrosisControlled releaseRho-associated protein kinaseMice Knockout0303 health sciencesDrug Carriersrho-Associated KinasesChemistryCIRRHOTIC RATS021001 nanoscience & nanotechnologyMicrospheresY-27632Drug deliveryFemale0210 nano-technologyDrug carrierATP Binding Cassette Transporter Subfamily BSIGNALING CONTRIBUTESLiver fibrosisBiologicalsHEPATIC STELLATE CELLSCell LineMECHANISMSReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesDELIVERYROCK INHIBITORmedicineAnimalsHumansProtein Kinase Inhibitors030304 developmental biologyProtein deliveryPORTAL PRESSUREmedicine.diseaseAmidesTargeted drug deliveryRho kinase inhibitorDelayed-Action PreparationsHepatic stellate cellVASODILATIONJournal of Controlled Release
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Exploring organ-specific features of fibrogenesis using murine precision-cut tissue slices

2019

Fibrosis is the hallmark of pathologic tissue remodelling in most chronic diseases. Despite advances in our understanding of the mechanisms of fibrosis, it remains uncured. Fibrogenic processes share conserved core cellular and molecular pathways across organs. In this study, we aimed to elucidate shared and organ-specific features of fibrosis using murine precision-cut tissue slices (PCTS) prepared from small intestine, liver and kidneys. PCTS displayed substantial differences in their baseline gene expression profiles: 70% of the extracellular matrix (ECM)-related genes were differentially expressed across the organs. Culture for 48 h induced significant changes in ECM regulation and trig…

Liver CirrhosisEXPRESSION0301 basic medicineINHIBITOR LY2157299 MONOHYDRATEPROTEINPrecision-cut tissue slicesSmad2 ProteinLIVER FIBROSISBiologyKidneyMECHANISMSSMAD2ACTIVATIONPATHWAYExtracellular matrixMiceTGFβ03 medical and health sciences0302 clinical medicineTransforming Growth Factor betaTGF betaFibrosisGene expressionTGF beta signaling pathwaymedicineAnimalsGalunisertibProtein Kinase InhibitorsMolecular BiologyMOLECULAR CHAPERONEGROWTH-FACTOR-BETAKinaseTGF-BETAExtracellular matrixmedicine.diseaseFibrosisPathophysiologyCell biologyMice Inbred C57BL030104 developmental biologyLiver030220 oncology & carcinogenesisQuinolinesPyrazolesMolecular MedicineCollagenHomeostasisSignal TransductionBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Novel therapeutic strategies for patients with NSCLC that do not respond to treatment with EGFR inhibitors

2014

Abstract: Introduction: Treatment with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) yields tumour responses in non-small cell lung cancer (NSCLC) patients harbouring activating EGFR mutations. However, even in long-lasting responses, resistance to EGFR TKIs invariably occurs. Areas covered: This review examines resistance mechanisms to EGFR TKI treatment, which mainly arise from secondary EGFR mutations. Other resistance-inducing processes include mesenchymal-epithelial transition factor (MET) amplification, epithelial-mesenchymal transformation, phenotypic change from NSCLC to small-cell lung carcinoma, and modifications in parallel signalling pathways. Current…

Lung NeoplasmsSettore MED/06 - Oncologia MedicaAfatinibNovel therapeutic strategiesLapatinibmedicine.disease_causeNSCLCT790Mchemistry.chemical_compoundErbB ReceptorsCarcinoma Non-Small-Cell LungAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansRadiology Nuclear Medicine and imagingEpidermal growth factor receptorProtein Kinase InhibitorsEGFR inhibitorsbiologybusiness.industryEGFR mutations; TKI inhibitors resistance; NSCLC; New drugs; Novel therapeutic strategiesGeneral MedicineNew drugEGFR mutationsCombined Modality TherapyDacomitinibrespiratory tract diseasesErbB ReceptorsNew drugsOncologychemistryDrug Resistance NeoplasmCancer researchbiology.proteinKRASHuman medicineEGFR mutationbusinessmedicine.drugTKI inhibitors resistanceCancer Treatment Reviews
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The role of cMET in non-small cell lung cancer resistant to EGFR-Inhibitors: Did we really find the target?

2014

Abstract: The advent of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) represented the most important innovation in NSCLC treatment over the last years. However, despite a great initial activity, secondary mutations in the same target, or different alterations in other molecular pathways, inevitably occur, leading to the emergence of acquired resistance, in median within the first year of treatment. In this scenario, the mesenchymal-epidermal transition (cMET) tyrosine kinase receptor and its natural ligand, the hepatocyte growth factor (HGF), seem to play an important role. Indeed either the overexpression or the amplification of cMET, as well as the overexpr…

Lung NeoplasmscMETcMET; cMET-Inhibitors; EGFR-TKIs resistance; HGF; NSCLC; Targeted therapies; Molecular Medicine; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Clinical BiochemistryClinical BiochemistryAntineoplastic AgentsBiologyPharmacologyNSCLCReceptor tyrosine kinaseTargeted therapiesCarcinoma Non-Small-Cell LungDrug DiscoverymedicineHumansEpidermal growth factor receptorHGFLung cancerProtein Kinase InhibitorsEGFR inhibitorsEGFR-TKIs resistancePharmacologyClinical Trials as TopicPharmacology. TherapyDrug Discovery3003 Pharmaceutical ScienceAntibodies MonoclonalProto-Oncogene Proteins c-metmedicine.diseaseMolecular medicinerespiratory tract diseasesErbB ReceptorsDrug Resistance NeoplasmProto-Oncogene Proteins c-metbiology.proteinCancer researchMolecular MedicineDrug Therapy CombinationHepatocyte growth factorcMET-InhibitorTargeted therapiecMET-InhibitorsTyrosine kinasemedicine.drug
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p38 MAPK-dependent shaping of the keratin cytoskeleton in cultured cells

2007

Plasticity of the resilient keratin intermediate filament cytoskeleton is an important prerequisite for epithelial tissue homeostasis. Here, the contribution of stress-activated p38 MAPK to keratin network organization was examined in cultured cells. It was observed that phosphorylated p38 colocalized with keratin granules that were rapidly formed in response to orthovanadate. The same p38p recruitment was noted during mitosis, in various stress situations and in cells producing mutant keratins. In all these situations keratin 8 became phosphorylated on S73, a well-known p38 target site. To demonstrate that p38-dependent keratin phosphorylation determines keratin organization, p38 activity …

MAP Kinase Signaling SystemIntermediate filament cytoskeletonmacromolecular substancesBiologyp38 Mitogen-Activated Protein KinasesArticleKeratinHumansPhosphorylationCytoskeletonProtein Kinase InhibitorsMitosisResearch ArticlesCells CulturedCytoskeletonchemistry.chemical_classificationKeratin Filamentintegumentary systemCell BiologyCell biologyKeratin 5chemistryKeratin 8KeratinsPhosphorylationVanadatesJournal of Cell Biology
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Evaluation and clinical analyses of downstream targets of the Akt inhibitor GDC-0068.

2013

Abstract Purpose: The oncogenic PI3K/Akt/mTOR pathway is an attractive therapeutic target in cancer. However, it is unknown whether the pathway blockade required for tumor growth inhibition is clinically achievable. Therefore, we conducted pharmacodynamic studies with GDC-0068, an ATP competitive, selective Akt1/2/3 inhibitor, in preclinical models and in patients treated with this compound. Experimental Design: We used a reverse phase protein array (RPPA) platform to identify a biomarker set indicative of Akt inhibition in cell lines and human-tumor xenografts, and correlated the degree of pathway inhibition with antitumor activity. Akt pathway activity was measured using this biomarker se…

MAPK/ERK pathwayCancer ResearchAKT1PharmacologyPiperazines03 medical and health sciencesMicePhosphatidylinositol 3-Kinases0302 clinical medicineIn vivoMedicineAnimalsHumansProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesbusiness.industryTOR Serine-Threonine KinasesCancerReverse phase protein lysate microarraymedicine.diseaseXenograft Model Antitumor Assays3. Good healthOncogene Protein v-aktPyrimidinesOncology030220 oncology & carcinogenesisBiomarker (medicine)businessSignal TransductionClinical cancer research : an official journal of the American Association for Cancer Research
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