15 results about "CD59" patented technology

The invention belongs to the technical field of biological medicines, and particularly relates to application of chenodeoxycholic acid in preparation of drugs for treating allergic diseases. It is found that CDCA can effectively inhibit pyroptosis and secretion of proinflammatory factors, expression of complement inhibition proteins CD46, CD55 and CD59 is remarkably up-regulated, expression of the complement inhibition proteins CD46, CD55 and CD59 is finally promoted, and occurrence and development of allergic diseases are effectively relieved. In a mouse model, CDCA can significantly improve OVA-induced food allergy symptoms, and has application prospects in treatment of allergic diseases.

The invention relates to the field of oncology, in particular to application of a cancer immunotherapy target and a diagnosis and prognosis prediction biomarker. Wherein at least one marker in the EGFR / Wnt / beta-catenin-LINC00973-miRNA-CD55 / CD59 pathway can be used for evaluating the sensitivity or the prognosis of the cancer immunotherapy.

The present invention relates to an oncolytic virus co-expressing the complement regulatory proteins CD55 and CD59. The oncolytic virus of the present invention maintains efficacy even upon intravenous injection, and thus, it may be applied to the therapy for various solid carcinomas and metastatic cancers as well as superficial solid cancers. In addition, the oncolytic virus of the present invention acquires resistance to the attack of human complement system by expressing a complement regulatory protein on the surface of the virus, and thus, it is stable in blood, and it maintains stable oncolytic activity upon intravenous injection, and thus, it may reduce the dose of the virus to minimize adverse effects of anticancer agents. Therefore, the oncolytic virus of the present invention may be advantageously used for prevention or treatment of cancer.

Applicants engineered peptide-modified AAV9 capsids for system-wide enhanced organ transduction by directly engineering a binding interaction with the human GPI-linked glycoprotein CD59. Adeno-associated vimses (AAVs) are used by numerous approved and investigational gene therapies. However, native AAVs have limited tissue tropisms and have comparatively low extrahepatic delivery efficiencies. While capsid engineering has largely focused on targeting specific organs, treating multisystem disorders requires efficient gene delivery to many organs. Here Applicants describe novel engineered capsids that bind CD59.

The invention belongs to the technical field of biological medicine, and particularly relates to a recombinant adeno-associated virus vector for delivering anti-VEGF (vascular endothelial growth factor) and complement protein co-expression and application of the recombinant adeno-associated virus vector. The co-expression system is constructed by adopting a genetic engineering technology, and efficient co-expression and accurate shearing of two treatment proteins are realized by inserting an F2A polypeptide connecting sequence between an Aflibercept protein coding sequence and a CD59 protein coding sequence.

This document provides methods and materials involved in reducing cardiac xenograft rejection. For example, methods and materials for preparing transgenic pigs expressing reduced or no endogenous Sda or SDa-like glycans derived from the porcine β1,4 N-acetyl-galactosaminyl transferase 2 (B4GALNT2) glycosyltransferase and / or reduced or no endogenous α-Gal antigens, methods and materials for modifying the xenograft recipient's immunological response to non-Gal antigens (e.g. CD46, CD59, CD9, PROCR, and ANXA2) to reduce cardiac xenograft rejection, and methods and materials for monitoring the progress of xenotransplant immunologic rejection are provided.

The invention pertains to treating a cognitive impairment, for example, an aging-associated cognitive impairment. In certain aspects, a sample obtained from a subject is assayed for the ratio between the levels of any two proteins selected from: DLL1, SMOC1, CD59, TSTD1, STAT3, POLD4, PARP11, LEFTY2, UNC5B, C5, C5.C6, ASH2L, INHBB, RSP3, VAV3, SIRT3 and SERPINB8. A subject may be having or suspected of having a cognitive impairment. The cognitive impairment can be caused by a neurodegenerative disease, such as Alzheimer's disease. A subject may be identified as likely or not likely to respond positively to the plasma exchange therapy based on the ratio between the levels of measured proteins. In certain aspects, methods for treating a cognitive impairment in the subject comprise administering a plasma exchange therapy comprising a full and / or low volume plasma exchange. Also provided are kits suitable for performing such methods.

This invention relates to an antibody composition for detecting PNH clones and its application. The antibody composition comprises a first antibody group, a second antibody group, and a third antibody group. The first antibody group includes a CD235a antibody, the second antibody group includes a CD235a antibody and a CD59 antibody, and the third antibody group includes a FLAER antibody, a CD157 antibody, a CD15 antibody, a CD64 antibody, and a CD45 antibody. In this invention, the three antibody groups can be used to identify mature erythrocytes, neutrophils, and monocytes in peripheral blood. PNH clones in erythrocytes are detected using CD235a and CD59, and PNH clones in neutrophils and monocytes are detected using FLAER and CD157 antibodies. The FLAER antibody directly binds to the GPI anchor structure, and the CD157 antibody, as an additional GPI anchor protein indicator, can detect potentially missed microclones.

The invention pertains to treating a cognitive impairment, for example, an aging-associated cognitive impairment. In certain aspects, a sample obtained from a subject is assayed for the ratio between the levels of any two proteins selected from: DLL1, SMOC1, CD59, TSTD1, STAT3, POLD4, PARP11, LEFTY2, UNC5B, C5, C5.C6, ASH2L, INHBB, RSP3, VAV3, SIRT3 and SERPINB8. A subject may be having or suspected of having a cognitive impairment. The cognitive impairment can be caused by a neurodegenerative disease, such as Alzheimer's disease. A subject may be identified as likely or not likely to respond positively to the plasma exchange therapy based on the ratio between the levels of measured proteins. In certain aspects, methods for treating a cognitive impairment in the subject comprise administering a plasma exchange therapy comprising a full and / or low volume plasma exchange. Also provided are kits suitable for performing such methods.

The application discloses application of a cancer immunotherapy target and a diagnosis, prognosis prediction biomarker, and determines detection of cancer cells of a patient or blood of the patient to contain: an EGFR activation level, a Wnt pathway activation level, an activated beta-catenin level, a long non-coding RNA LINC00973 expression level, a LNC1574203 expression level, a CD55 protein and mRNA expression level, a CD59 protein and mRNA expression level, and a CD73 protein and mRNA expression level, which are higher than reference levels, are used for diagnosis, prognosis prediction and treatment of cancer.

Applicants engineered peptide-modified AAV9 capsids for system-wide enhanced organ transduction by directly engineering a binding interaction with the human GPI-linked glycoprotein CD59. Adeno-associated vimses (AAVs) are used by numerous approved and investigational gene therapies. However, native AAVs have limited tissue tropisms and have comparatively low extrahepatic delivery efficiencies. While capsid engineering has largely focused on targeting specific organs, treating multisystem disorders requires efficient gene delivery to many organs. Here Applicants describe novel engineered capsids that bind CD59.

Applicants engineered peptide-modified AAV9 capsids for system-wide enhanced organ transduction by directly engineering a binding interaction with the human GPI-linked glycoprotein CD59. Adeno-associated vimses (AAVs) are used by numerous approved and investigational gene therapies. However, native AAVs have limited tissue tropisms and have comparatively low extrahepatic delivery efficiencies. While capsid engineering has largely focused on targeting specific organs, treating multisystem disorders requires efficient gene delivery to many organs. Here Applicants describe novel engineered capsids that bind CD59.

Disclosed herein are polynucleotides encoding fusion proteins, the fusion proteins comprising a vaccinia virus envelope protein, such as A13 or part thereof and at least one complement regulatory protein, such as CD35, CD55, CD59, CD46, CR1, Factor H, VCP, MOPICE, SPICE and CCPH, or a functional fragment thereof. Modified vaccinia virus vectors and vaccinia virus virions are also disclosed, as are therapeutic uses and methods for treatment of cancers and / or proliferative diseases or disorders.

The present invention relates to an oncolytic virus co-expressing the complement regulatory proteins CD55 and CD59. The oncolytic virus of the present invention maintains efficacy even upon intravenous injection, and thus, it may be applied to the therapy for various solid carcinomas and metastatic cancers as well as superficial solid cancers. In addition, the oncolytic virus of the present invention acquires resistance to the attack of human complement system by expressing a complement regulatory protein on the surface of the virus, and thus, it is stable in blood, and it maintains stable oncolytic activity upon intravenous injection, and thus, it may reduce the dose of the virus to minimize adverse effects of anticancer agents. Therefore, the oncolytic virus of the present invention may be advantageously used for prevention or treatment of cancer.

Compositions and kits for diagnosing and prognosing Alzheimer's Disease (AD) in a human patient include a binding agent such as a monoclonal antibody for a biomarker conjugated to a detectable moiety such as a fluorophore, wherein the biomarker is chosen from CD163, CD91, CD59, MerTK and other phagocytosis-related molecules. Further compositions and kits employ panels of fluorophore-conjugated monoclonal antibodies for biomarkers including scavenger receptors. Methods for determining the relative expression of biomarkers, diagnosing AD, and determining the efficacy of AD therapeutic candidates such as phagocytosis-promoting agents and scavenger receptor agonists also appear.