Human Anti-WISP1 Antibodies for Treatment of Idiopathic Pulmonary Fbrosis
用于治疗特发性肺纤维化的人抗 WISP1 抗体
基本信息
- 批准号:8785946
- 负责人:
- 金额:$ 22.48万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2014
- 资助国家:美国
- 起止时间:2014-08-18 至 2016-02-29
- 项目状态:已结题
- 来源:
- 关键词:AddressAerosolsAffectAlveolarAmericanAntibodiesAttenuatedBackBleomycinCellsCicatrixClinicalCollaborationsComorbidityCoughingDataDepositionDevelopmentDiseaseDrug Delivery SystemsDrug KineticsEpithelialEpithelial CellsEtiologyEvaluationEventExerciseExtracellular MatrixFDA approvedFatal OutcomeFibroblastsFibrosisFutureGrowth FactorHamman-Rich syndromeHumanHyperplasiaImmunotherapyIn VitroIntravenousKineticsLeft lungLibrariesLifeLife ExpectancyLungLung TransplantationMatrix MetalloproteinasesMediatingMesenchymalModelingMonoclonal AntibodiesOutcomePathway interactionsPharmaceutical PreparationsPharmacologic SubstancePhaseProcessProductionPulmonary FibrosisPulmonologyRegulationRespiratory FailureRiskRouteSafetyShortness of BreathSignal TransductionSignaling ProteinSolidStimulusStructure of parenchyma of lungSurfaceSymptomsSyndromeTherapeuticTissuesUniversitiesWISP1 geneWNT1 geneanalytical methodautocrinebasebiophysical propertiescandidate identificationcell injurydesigndrug developmentextracellularhuman WISP1 proteinin vivomethod developmentmigrationneutralizing antibodynovelparacrinepre-clinicalpublic health relevanceresearch study
项目摘要
DESCRIPTION (provided by applicant): New anti-fibrotic drugs are needed to treat Idiopathic Pulmonary Fibrosis (IPF). IPF is a progressive, chronically debilitating clinical syndrome with unknown etiology and a terminal outcome. IPF symptoms include persistent cough, progressive severe shortness of breath and decreased exercise capacity. Up to 200,000 Americans suffer from this disease with expected survival limited to 3-5 years. There are currently no approved US drugs leaving lung transplantation as the only option to extend life. IPF is initially characterized by alveolar epithelial cell injury followed by epithelial-mesenchymal transition (EMT) and exaggerated fibroblast migration, activation and proliferation with extracellular matrix deposition and tissue remodeling. When a sufficient proportion of the IPF lung becomes scarred respiratory failure and comorbidities occur. WNT1- Inducible Signaling Protein-1 (WISP1; also known as CCN4) is an autocrine and paracrine extracellular stimulus for EMT. Studies have shown that: 1. WISP1 is induced in human lung cells by TGF-¿; 2. WISP1 is upregulated at the alveolar epithelial surface in IPF; 3. WISP1 protein stimulates EMT and fibroblast ECM deposition in vitro; 4. depletion of WISP1 with neutralizing antibodies attenuates bleomycin-induced pulmonary fibrosis in vivo. Currently, no IPF drugs are in development that target WISP1 or the WNT pathway. Together with our collaborators we have outlined experiments that will harness a powerful combination of antibody discovery, fibrotic pathway expertise and aerosol drug development to provide a solid basis for the discovery, evaluation and development of an anti-WISP1 immunotherapy for IPF treatment.
描述(申请人提供):治疗特发性肺纤维化(IPF)需要新的抗纤维化药物。特发性肺间质纤维化是一种进行性、慢性衰弱的临床综合征,病因不明,结局不详。IPF症状包括持续咳嗽、进行性严重呼吸急促和运动能力下降。多达20万美国人患有这种疾病,预计存活时间仅为3-5年。目前还没有批准的美国药物,使肺移植成为延长生命的唯一选择。IPF以肺泡上皮细胞损伤、上皮-间充质转化(EMT)、成纤维细胞过度迁移、活化和增殖、细胞外基质沉积和组织重塑为主要特征。当足够比例的IPF肺形成疤痕时,就会发生呼吸衰竭和合并症。WNT1诱导信号蛋白-1(WISP1;又称CCN4)是EMT的一种自分泌和旁分泌细胞外刺激因子。研究表明:1.转化生长因子β可诱导人肺泡上皮细胞表达WISP1;2.肺间质纤维化时肺泡上皮细胞表面WISP1表达上调;3.WISP1蛋白在体外可促进EMT和成纤维细胞ECM的沉积;4.用中和抗体去除WISP1可减轻博莱霉素诱导的体内肺纤维化。目前,还没有针对WISP1或WNT途径的IPF药物在开发中。我们与我们的合作者一起概述了实验,这些实验将利用抗体发现、纤维化途径专业知识和气雾剂药物开发的强大组合,为发现、评估和开发用于IPF治疗的抗WISP1免疫疗法提供坚实的基础。
项目成果
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Gunnar Joerg Floris Kaufmann其他文献
Gunnar Joerg Floris Kaufmann的其他文献
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