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公开(公告)号:US20180296703A1
公开(公告)日:2018-10-18
申请号:US15753003
申请日:2016-08-17
Inventor: Arthur M. FELDMAN , Joseph Y. CHEUNG
Abstract: The present invention features methods and compositions for treatment of heart failure. The compositions can include an isolated nucleic acid encoding a BAG3 polypeptide or fragment thereof.
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公开(公告)号:US20210254159A1
公开(公告)日:2021-08-19
申请号:US16973353
申请日:2019-06-07
Inventor: Arthur M. FELDMAN
IPC: C12Q1/6883 , A61K48/00
Abstract: Identification of BAG3 (Bcl2-associated anthanogene 3) genetic variants were associated with the prevalence non-ischemic or ischemic dilated cardiomyopathy (DCM) and DCM outcomes in individuals of African ancestry.
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公开(公告)号:US20170016066A1
公开(公告)日:2017-01-19
申请号:US15115807
申请日:2015-01-30
Inventor: Arthur M. FELDMAN , Douglas G. TILLEY , Weizhong ZHU , Kamel KHALILI , Walter J. KOCH
CPC classification number: C12Q1/6883 , A61K48/00 , C12Q2600/106 , C12Q2600/156 , C12Q2600/158 , G01N33/6887 , G01N33/6893 , G01N2500/04 , G01N2500/10 , G01N2800/325 , G01N2800/50
Abstract: Compositions are directed to BCL2-associated athanogene 3 (BAG3) molecules and agents which modulate expression of BAG3 molecules. Pharmaceutical composition for administration to patients, for example, patients with heart failure, comprise one or more BAG3 molecules or agents which modulate expression of BAG3. Methods of treatment and identifying candidate therapeutic agents are also provided.
Abstract translation: 组合物针对BCL2相关的athanogene 3(BAG3)分子和调节BAG3分子表达的试剂。 用于给予患者的药物组合物,例如患有心力衰竭的患者,包含调节BAG3表达的一种或多种BAG3分子或试剂。 还提供了治疗和鉴定候选治疗剂的方法。
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公开(公告)号:US20250001014A1
公开(公告)日:2025-01-02
申请号:US18736260
申请日:2024-06-06
Inventor: Arthur M. FELDMAN , Joseph Y. CHEUNG
Abstract: The present invention features methods and compositions for treatment of heart failure. The compositions can include an isolated nucleic acid encoding a BAG3 polypeptide or fragment thereof.
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公开(公告)号:US20230390357A1
公开(公告)日:2023-12-07
申请号:US18052863
申请日:2022-11-04
Inventor: Arthur M. FELDMAN , Joseph Y. CHEUNG , Kamel KHALILI
CPC classification number: A61K38/1709 , A61K31/69 , A61K45/06 , A61K38/05 , A61P9/10 , A61K9/0019 , C12N15/85
Abstract: The invention provides methods of treating ischemia/reperfusion injury in a subject. In one example, a method comprises administering a therapeutically effective amount of a pharmaceutical composition that increases levels of Bcl2-associated athanogene 3 (BAG3) polypeptide in ischemic tissue. The invention also provides methods of treating a subject at risk of ischemia/reperfusion injury. In one example, a method comprises administering a therapeutically effective amount of a pharmaceutical composition that increases levels of Bcl2-associated athanogene 3 (BAG3) polypeptide. In the invention methods, in one example, a pharmaceutical composition comprises a nucleic acid encoding BAG3 polypeptide.
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公开(公告)号:US20230241162A1
公开(公告)日:2023-08-03
申请号:US17971477
申请日:2022-10-21
Applicant: Temple University of the Commonwealth System of Higher Education , Loyola University of Chicago
Inventor: Arthur M. FELDMAN , Jonathan KIRK
CPC classification number: A61K38/1709 , A61K48/0058 , A61K48/0066 , A61P29/00 , A61P9/00
Abstract: Bag3 is a multifunctional protein expressed predominantly in the heart, the skeletal muscle, the central nervous system and in many cancers. Although BAG3 was cloned only a decade ago, studies have shown that genetic variants, particularly those that result in haplo-insufficiency, can lead to severe left ventricular dysfunction; however, the full mechanisms responsible have remained obscure. To obviate the influence of heart failure itself on the biology of Bag3, ransgenic mice harboring a single allele knock-out were studied between 8 and 10 weeks of age before any obvious signs of heart failure were evident. The results were surprising and informative. First, it was found that despite a normal phenotype, young Bag3+/− had marked changes in the proteome that were characterized by changes in proteins associated with metabolism and apoptosis. Consistent with this finding, a decrease in the levels of critical proteins charged with maintaining the mitochondrial membrane potential was observed. It was also found that young mice shifted from a balance between the extrinsic and intrinsic pathways of apoptosis. However, in the presence of stress and the absence of Bag3 there was a shift from a balanced to an extrinsic dominant system (cleaved caspase 8). The diverse array of critical pathways regulated by Bag3 suggests a more important role especially during stress and that this role might include serving as an intracellular glue that holds proteins where they can be most effective rather than having them meet accidentally.
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