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Targeting cancer cachexia drivers using antibody-based approaches
Organization VIRGINIA COMMONWEALTH UNIVERSITYLocation RICHMOND, UNITED STATESPosted 11 Dec 2023Deadline 31 Mar 2025 β οΈ
NIHUS FederalResearch GrantFY2025AblationAccelerationAntibodiesBi-specific antibodiesBifunctional AntibodiesBindingBispecific AntibodiesBispecific Monoclonal AntibodiesBody Weight decreasedCDK4ICDKN2CDKN2 GenesCDKN2ACDKN2A geneCMM2CachecticCachectin ReceptorsCachexiaCancer CachexiaCancer PatientCell BodyCell Communication and SignalingCell SignalingCellsCessation of lifeComplicationCyclin-Dependent Kinase Inhibitor 2A GeneDeathDiseaseDisorderDoseDrug toxicityDysfunctionEmbryoEmbryonicEpidermal Growth Factor-Related Transforming Growth FactorEpitheliumEventFibroblastsFunctional disorderGene ExpressionGenesGeneticHeterozygoteINK4INK4AIncidenceIndividualInflammationInflammatoryInflammatory ResponseIntracellular Communication and SignalingKRAS(G12D)KRASG12DLeadLifeMTS1MTS1 GenesMalignant CellMalignant Pancreatic NeoplasmMalignant neoplasm of pancreasMediatingMembraneMiceMice MammalsModelingMolecular InteractionMurineMusMuscleMuscle AtrophyMuscle TissueMuscle functionMuscular AtrophyNuclearOrganOutcomePDAC cancer cellPDAC cellPancreasPancreas CancerPancreas Ductal AdenocarcinomaPancreaticPancreatic CancerPancreatic Ductal AdenocarcinomaPatient outcomePatient-Centered OutcomesPatient-Focused OutcomesPatientsPb elementPhenotypePhysiopathologyQOLQuality of lifeRNA SeqRNA sequencingRNAseqReceptor ProteinRecombinantsReportingResistance developmentResistant developmentRoleSignal TransductionSignal Transduction SystemsSignalingSkeletal MuscleSyndromeTGF ATGF-alphaTGF-Ξ±TGFalphaTGFΞ±TNF Receptor Family ProteinTNF Receptor SuperfamilyTNF ReceptorsTNFRTP16TSG9ATestingTherapeuticTransforming Growth Factor alphaTransgenesTreatment EfficacyTumor CellTumor Necrosis Factor ReceptorTumor Necrosis Factor Receptor FamilyTumor Necrosis Factor Receptor SuperfamilyVoluntary MuscleWasting DiseaseWasting SyndromeWeight LossWeight Reductionbi-specific monoclonal antibodiesbiological signal transductionbody weight lossbsAbcancer associated cachexiacancer cellcancer induced cachexiacancer-associated muscle wastingcancer-induced muscle atrophycancer-induced muscle losscancer-induced muscle wastingcancer-related cachexiacombatdecreased muscle massdesigndesigningdeveloping resistanceexperimentexperimental researchexperimental studyexperimentsheavy metal Pbheavy metal leadheterozygosityhuman modelimprovedinnovateinnovationinnovativeinsightintervention efficacylow muscle massmembrane structuremodel of humanmouse modelmurine modelmuscle breakdownmuscle bulkmuscle degradationmuscle deteriorationmuscle formmuscle lossmuscle massmuscle strengthmuscle wastingmuscularmutantneoplastic cellnew drug treatmentsnew drugsnew pharmacological therapeuticnew therapeuticsnew therapynext generation therapeuticsnovel drug treatmentsnovel drugsnovel pharmaco-therapeuticnovel pharmacological therapeuticnovel therapeuticsnovel therapyoverexpressoverexpressionp14ARFp16 Genesp16INK4 Genesp16INK4A Genesp16INK4apancreatic cancer cellspancreatic ductal adenocarcinoma cellpancreatic malignancypancreatic tumor cellspathophysiologypatient oriented outcomespharmacologicreceptorreduced muscle masssocial roletherapeutic efficacytherapeutic evaluationtherapeutic testingtherapy efficacytranscriptome sequencingtranscriptomic sequencingtransgenetranslational opportunitiestranslational potentialtumor-induced cachexiatumor-induced muscle wastingvirtualwasting conditionwasting disorderwt-loss
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PROJECT SUMMARY
Cancer-associated cachexia is a debilitated syndrome that has a dramatic impact on the quality of life and
outcome of patients. Cancer cachexia occurs with a remarkably high incidence in pancreatic ductal
adenocarcinoma (PDAC) patients. Cancer cachexia is characterized by the progressive depletion of muscle
skeletal mass, whichβ¦
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