70 results about "CD24" patented technology

The invention discloses an anti-CD24 antibody and an application thereof. Specifically disclosed is an anti-CD24 antibody or antigen-binding fragment thereof, comprising a heavy chain variable region (SEQ ID NO: 1, 5, 9 or 13) and a light chain variable region (SEQ ID NO: 3, 7, 11 or 15). The anti-CD24 antibody (including a mouse monoclonal antibody and three humanized monoclonal antibodies) is obtained through a hybridoma technology and a CDR transplantation method. The anti-CD24 antibody has high affinity, can significantly inhibit the growth of tumors, has a tumor inhibition rate of 82.3%, has a significant anti-tumor curative effect, has a strong binding capacity with various tumor cells and tissues, does not bind with normal cells, and has good tumor selectivity. The antibody can be prepared into prevention and treatment drugs, diagnosis drugs, detection kits and the like for CD24 target related diseases, and has very wide clinical application prospects in the fields of tumor treatment and diagnosis and the like.

Provided is an antibody fusion protein, which simultaneously targets CD24, IL4R and an integrin receptor. An in-vitro assay shows that the antibody fusion protein significantly inhibits the proliferation, migration, invasion, colony formation and adhesion of renal cancer cells, also has a comprehensive and significant anti-tumor effect on gastric cancer, colon cancer and breast cancer, and has the effect of inhibiting angiogenesis. The results of a mouse tumor model of subcutaneous transplantation of MC38-hPDL1C57BL6 / J show that the antibody fusion protein combined with the PDL1 antagonist atezolizumab can significantly inhibit tumor growth. The antibody fusion protein can be used as a potential candidate drug for treating metastatic renal cell carcinoma, PDL1-overexpressing cancer, ophthalmic diseases and inflammation or autoimmune diseases.

CD24-positive malignant and benign tumors are treated by administration of a naturally occurring or modified oncolytic Zika virus. Diseases associated with abnormal T cell activation or T cell-mediated autoimmunity, wherein CD24 expression is increased, are also expected to be treated by administration of a naturally occurring or modified oncolytic Zika virus. Also contemplated are compounds and methods for treating and / or preventing Zika virus infection in a subject.

Disclosed are a CD24 antibody or an antigen-binding fragment thereof and the medical use thereof. Further, disclosed are a chimeric antibody comprising CDRs of the CD24 antibody, a humanized antibody, a pharmaceutical composition comprising the CD24 antibody or the antigen-binding fragment thereof, and the use thereof as an anticancer drug.

The present invention relates to a novel anti-CD24 antibody and use thereof. The CD24-specific antibody according to one aspect increases phagocytosis activity of macrophages in tumor tissues, and thus can be used as a universal anticancer agent for effectively preventing or treating various cancers associated with CD24 without being limited to carcinomas, and has high binding affinity to both humans and mice, and thus can be clinically and preclinically used.

The invention discloses a diagnostic marker for ANCA (Angiovasculitis) related vasculitis. It is found for the first time that the CD19 + CD38 + CD27-CD24 + cell can be used as the diagnosis marker of ANCA related vasculitis, and the diagnosis efficiency is high; in addition, it is found that the CD19 + CD38 + CD27-CD24 + cells can remarkably distinguish ANCA related vasculitis and membranous nephropathy or ANCA related vasculitis and lupus nephritis, a new direction is provided for diagnosis and subsequent treatment of ANCA related vasculitis, and the application has wide application prospects clinically.

To provide a cell including a cell expressing CD24, and related method of use and creation thereof.SOLUTION: Provided is an isolated cell including modification for increasing reduced expression of MHC class I and / or MHC class II human leukocyte antigens and expression of CD24 in a cell. In some embodiments, the cell includes reduced expression of MHC class I and MHC class II human leukocyte antigens.SELECTED DRAWING: None

The invention discloses a bispecific antibody coupling drug targeting CD24 and HER2 and a preparation method and application thereof.The bispecific antibody coupling drug comprises an anti-CD24 heavy chain, an anti-CD24 light chain, an anti-HER2 heavy chain, an anti-HER2 light chain, a tetrapeptide linker and a topoisomerase I inhibitor exatan derivative, the DAR value of the bispecific antibody coupling drug is 9.25, and the anti-CD24 heavy chain, the anti-HER2 light chain, the tetrapeptide linker and the topoisomerase I inhibitor exatan derivative are different. The compound has strong cytotoxicity and internalization ability on breast cancer cells, not only can specifically target tumor tissues, but also can release drugs to kill target cells and adjacent tumor cells, and can significantly inhibit growth of breast cancer tumors. An antibody part DACH023 in the bispecific antibody coupling medicine is the same as a traditional IgG molecule, a traditional monoclonal antibody structure is reserved to the maximum extent, due to the existence of an Fc fragment, a common Protein A column affinity chromatography method can be adopted for purification, and large-scale production and purification are facilitated.

Provided are multispecific antibodies or fragments thereof having binding specificity to the human CD24 protein. Methods of using the antibodies or fragments thereof for treating cancer, autoimmune disease or inflammatory condition are also provided.

This invention provides a CD24-targeted nanomedicine delivery system and its application in the preparation of antitumor drugs. The nanomedicine delivery system of this invention comprises (1) a core structure: mesoporous manganese dioxide (hMnO₂) for co-loading glucose oxidase (GOx) and cysteine ​​(Cys); and (2) targeted delivery: nanoparticles encapsulated in a genetically engineered membrane EM-CD24 modified with the anti-CD24 single-chain variable fragment scFv. This invention can improve tumor penetration, reduce off-target accumulation, and enhance pharmacokinetics, achieving therapeutic Gox and cysteine ​​concentrations in the tumor while maintaining low systemic exposure, thus minimizing off-target toxicity.

The application discloses humanized anti-CD24 antibodies and application thereof, relates to the technical field of biological medicine, and specifically provides humanized antibodies capable of specifically recognizing CD24 and application thereof. FR regions and constant regions of a mouse-derived anti-CD24 monoclonal antibody are replaced by human-derived FR regions and constant regions, and CDR of the variable region of the mouse-derived anti-CD24 monoclonal antibody is retained, so that a series of anti-CD24 humanized monoclonal antibodies are obtained. The humanized antibodies obtained by the application have an affinity to CD24 antigens which is basically equivalent to that of a human-mouse chimeric anti-CD24 monoclonal antibody WT, and exhibit strong anti-tumor capacity in vivo.

The invention discloses an inflammatory bowel disease treatment method based on intestinal flora regulatory gene CD24 expression. According to the method, expression or functions of CD24 in host intestinal epithelial cells are up-regulated, the intestinal flora structure is adjusted, and intestinal inflammation is relieved. CD24 up-regulation can be realized by transfecting a CD24 gene overexpression vector, applying a transcription factor or a small molecule agonist or enhancing the activity of an endogenous gene by utilizing a gene editing technology. The CD24 is regulated and controlled, so that the proportion of the phylum firmicalis to the phylum bacteroides can be normalized, the enrichment of short-chain fatty acid producing flora is promoted, the activation of NF-kappa B and NLRP3 inflammasomes is inhibited, and the intestinal barrier function is enhanced. The DSS induced colitis model is established by drinking a 2-5% dextran sodium sulfate solution by a mouse, and simulates the pathological characteristics of human ulcerative colitis. Intervention modes include oral administration, enema or nanoparticle targeted delivery of the CD24 agonist pharmaceutical composition. The invention provides a new strategy for the treatment of inflammatory bowel diseases, especially ulcerative colitis, and has obvious dual curative effects of anti-inflammation and flora regulation.

The invention provides an engineering exosome drug delivery system for over-expression of CD24 and a preparation method thereof, and belongs to the technical field of gene engineering. CD24 is overexpressed on a membrane of the engineered exosome, and a gene sequence of a plasmid of the overexpressed CD24 is as shown in SEQ ID No. 1; a CD24 sequence is fused to the N end of an I-type transmembrane protein structure LAMP2B on a membrane of the engineered exosome, a glycosylation sequence GNSTM is introduced to the N end of the fusion sequence, and an exosome binding peptide Signal peptide fragment is fused to the N end of the glycosylation sequence GNSTM. The engineering exosome for over-expressing CD24 on an exosome membrane is successfully constructed by using a fusion gene for coding transmembrane proteins LAMP2B and CD24, the aggregation and protein adsorption phenomena of the engineering exosome can be effectively retarded, the drug delivery targeting of the engineering exosome is enhanced, the in-vivo duration of the engineering exosome is prolonged, and the delivery performance of the engineering exosome is further improved.

Disclosed is a method for preparing a universal cell. After major histocompatibility complex class I (MHC-I) and class II genes are inactivated in cells, fusion proteins comprising functional domains of CD47 and / or CD24 are overexpressed, such that the obtained human pluripotent stem cells or human cell lines can, on the basis of escaping T cell attack, further escape killing by NK cells, the effect of which is even better than that of the reported stellar target CD47. Meanwhile, the pluripotent stem cells with low immunogenicity retain their stemness and differentiation capacity.

The invention discloses a CD24-knockout lung cancer cell line as well as a construction method and application thereof. According to the invention, sgRNA specifically targeting human CD24 is firstly designed, and CD24 genes in human lung cancer cell lines PC-9, HCC827 and H1975 cells are successfully knocked out through a CRISPR-Cas9 gene editing technology. Protein expression is detected through Western blot, and Sanger sequencing is carried out, so that the success of knockout cell construction is proved. The lung cancer cell line can be used for researching the action mechanism of CD24 in lung cancer; and an anti-lung cancer drug for screening the targeted CD24. Therefore, the cell line can be widely applied to scientific research and clinical related basic research.

Chimeric antigen receptors that bind to CD24, optionally further including CXCR3 or IL-15, and optionally further including EGFRt, polynucleotides encoding the receptors, cells comprising the polynucleotides, and methods of treating cancers using said chimeric antigen receptors or cells are disclosed.

GITRL+ IgDlow / − B cells as well as methods of making and using said cells are described herein. Also described are methods for treating an autoimmune disease or an inflammatory condition in a subject in need thereof of using said B cells. The B cells may be GITRL+ IgDlowCCR7+ CXCR5+ B cells or GITRL+ IgDlow CCR7+ CXCR5+ CD23+ CD24+ B cells.

The invention discloses a nerve cell differentiated from an immunoprivilege induced pluripotent stem cell and an application thereof. After main histocompatibility complex HLA-I and II type genes are inactivated in induced pluripotent stem cells, fusion protein XSG006 constructed by functional structural domains of CD47 and CD24 is over-expressed, the obtained induced pluripotent stem cells are differentiated to obtain separated low-immunogenicity dopaminergic neural precursor cells, and the low-immunogenicity dopaminergic neural precursor cells can be used for preparing the low-immunogenicity dopaminergic neural precursor cells on the basis of attack of escape T cells. And further, the NK cells and macrophages are escaped for killing. And attacks of an immune system can be effectively escaped in vivo. In a mouse Parkinson's disease model and a non-human primate (NHP) Parkinson's disease model, the strain can continuously survive in a host for a long time and generate activity, and the Parkinson's disease is fundamentally reversed. And an experimental basis and a theoretical basis are provided for establishing a PD treatment strategy and designing a novel stem cell treatment medicine.

The invention discloses a method for identifying chronic granulocyte immune typing by using a flow cytometer. The method comprises the following steps: incubating and purifying a to-be-detected sample and a fluorescein-labeled antibody composition; the method comprises the following steps: carrying out flow cytometry detection on resuspended cells: firstly, circling a liquid flow stable interval by utilizing Time / CD45, FSC INT / PEAK and FSC INT / SSC INT scatter diagrams, and removing sticky bodies and cell debris; all leukocyte groups are circled through combination of CD45 and SSC, and mononuclear cells are circled in all leukocyte gates through CD45 / SSC gate setting; excluding CD 19 + B lymphocytes; cD7 + T and NK cells are excluded; cD2 + T and NK cells are eliminated; immature and mature granulocytes of CD 16 and CD24 < + > are excluded through CD 16 / CD24 gate setting; the method comprises the following steps of: screening CD14-CD16, removing basophilic granulocytes of CD14-CD16-and residual NK (Natural Killer) cells, dividing a cross gate to determine the proportion of CD 14 + CD16-cMo cells, CD 14 + CD16 + iMo cells and CD 16 + CD 14 ncMo cells, and determining the proportion of the CD14 + CD16-cMo cells, the CD14 + CD16 + iMo cells and the CD16 + CD14 ncMo cells; cD34 / SSC gate setting is carried out, and CD34 + original cells are circled to calculate the proportion.

The invention belongs to the field of biological medicine, and particularly discloses a culture method of domesticated mesenchymal stem cells (MSCs), which comprises the following steps: separating plasma and platelet lysis buffer from autologous peripheral blood, and obtaining CTL and Treg through magnetic bead sorting; the method comprises the following steps: sequentially co-culturing umbilical cord MSCs for three generations: co-culturing the P1 generation and CTL in a culture medium containing 30% of alpha MEM, 68% of DMEM / F12, 1% of autologous plasma and 1% of platelet lysis buffer, and adding 0.1-1 [mu] M of resveratrol and 10-50 [mu] M of spermidine; co-culturing P2 and Treg in a culture medium containing 50% of alpha MEM, 48% of DMEM / F12, 1% of autologous plasma and 1% of platelet lysis buffer; the P3 generation is cultured and harvested in 90% of alpha MEM, 5% of DMEM / F12 and 5% of PRP. The obtained MSCs surface marker is CD105 < + > / CD90 < + > / CD73 < + > / CD45 <-> / CD34 <-> / HLA-DR <->, the expression quantity of CD24 is low (CD24low), the expression quantity of CD47 is high (CD47high), the expression quantity of PD-L1 is high (PD-L1 high), the IDO activity is larger than or equal to 25 U / mg, the retention rate of the lung after vein transplantation is smaller than or equal to 12%, and the survival period is larger than or equal to 28 days. The cell is suitable for treating ARDS or hepatic fibrosis.

This invention relates to compounds, compositions and methods for treating, reversing or preventing cancer through the modulation of immune responses via Killer-specific Secretory Protein 37 (Ksp37). By enhancing immune recognition, Ksp37 downregulates the checkpoint proteins CD47 and CD24 on abnormal cells, allowing the immune system to effectively identify and eliminate cancerous cells. Additionally, Ksp37 influences cytokine signalling by increasing IL-12 and decreasing IL-2 levels, which supports the activation of natural killer (NK) cells while mitigating chronic inflammation, fostering an immune environment conducive to clearing abnormal cells.

Provided are neutrophils and monocytes having unique combinations of cell surface markers capable of enhancing TRAMlo neutrophil or monocyte subsets, or capable of reprogramming neutrophils and monocytes into TRAM deficient neutrophils and monocytes, including methods of isolating the neutrophils and monocytes for use in treating chronic inflammatory diseases. The enhanced or reprogramed neutrophils may express surface markers comprising CD177lo and at least one of Dectin2 (Clec4n)lo, EHD1lo, CD84hi, Ly6E / Ly6Ahi, CD200Rhi, CD24hi, CD49Dlo, or a combination thereof, and the enhanced or reprogrammed monocytes may express surface markers comprising CD14+, CD16+, and at least one of CD24hi, CD200Rhi, or CD84hi.

The present disclosure relates generally to immunoglobulin-related compositions (e.g., antibodies or antigen binding fragments thereof) that can bind to the CD24 protein. The antibodies of the present technology are useful in methods for detecting and treating a CD24-associated cancer in a subject in need thereof.

A group of CD24-binding proteins and their uses are provided. Specifically, a group of antigen-binding proteins is provided in which cells expressing the antigen-binding protein may have cytotoxicity and safety. The use of antigen-binding proteins in the preparation of pharmaceuticals is also provided.

The invention discloses a chimeric antigen receptor constructed based on Siglec10, an immune cell and a preparation method and application of the chimeric antigen receptor and the immune cell, relates to the technical field of cellular immunity, and discloses a chimeric antigen receptor constructed through a targeted CD24-Siglec10 signal axis, and CAR-T, CAR-M and CAR-NK cells and the like constructed based on the receptor. By targeting a CD24-Siglec10 signal axis and integrating a natural receptor-ligand recognition mode and multi-signal domain collaborative design, the defects of antigen escape, TME inhibition and safety of a traditional CAR therapy in solid tumors are systematically solved, and an efficient, accurate and industrialized tumor immunotherapy new strategy is provided for clinical research.

This invention relates to the application of targeting the ABHD17C-BCL6B-CD24 signaling axis in the preparation of pancreatic cancer treatment products, the products comprising diagnostic reagents and targeted drugs. The diagnostic reagent kit contains at least one of the following: a reagent for detecting ABHD17C, a reagent for detecting BCL6B expression, and a reagent for detecting CD24 expression. The targeted drug for improving the efficacy and prognosis of pancreatic cancer treatment contains at least one of the following: a reagent for inhibiting ABHD17C expression, a reagent for inhibiting BCL6B expression, and a reagent for inhibiting CD24 expression. This invention reveals the mechanism by which the ABHD17C-BCL6B-CD24 signaling axis regulates pancreatic cancer, providing a theoretical basis for the precise diagnosis and targeted therapy of pancreatic cancer, and has broad clinical application prospects.

The invention belongs to the technical field of genetic engineering and biological medicine, and particularly discloses polypeptide self-assembled nanoparticles as well as a preparation method and application thereof. The polypeptide self-assembled nano-particle provided by the invention is mainly constructed by amphiphilic compound molecules based on polypeptide, and comprises two functional polypeptides: a targeting peptide (CR) based on tumor tissue high expression CXCR4, used for realizing precise targeting on tumor; a CD24 blocking peptide (CB) containing an MMP-2 responsive restriction enzyme cutting site releases LAG-CSBP polypeptide under the action of MMP-2 in a tumor microenvironment, so that the interaction of CD24 / Siglec-10 is blocked. Under the hydrophobic action force, a hydrophobic SLC7A11 inhibitor erastin is encapsulated by the two, and the nano-particles CBR and E are formed through self-assembly. According to the system, the tumor radiotherapy tolerance can be improved through multiple synergistic effects, and the treatment accuracy and safety are improved.

Provided herein are antibody-drug conjugates containing an anti-CD24 antibody conjugated to a cytotoxic agent via a linker, in which the antibody selectively binds to human CD24 protein expressed on cancer cells but not human CD24 expressed in non-cancerous cells; and uses thereof for treating cancer.

The present invention provided an isolated antibody, which specifically binds to human CD24, wherein the isolated antibody comprises: (a) a heavy chain variable region-complementarity determining region 1 (VH-CDR1), a VH-CDR2 and a VH-CDR3, wherein the VH-CDR1 consists of the amino acid sequence of SEQ ID NO: 2, the VH-CDR2 consists of the amino acid sequence of SEQ ID NO: 4, and the VH-CDR3 consists of the amino acid sequence of SEQ ID NO: 6; and (b) a light chain variable region-complementarity determining region 1 (VL-CDR1), a VL-CDR2 and a VL-CDR3, wherein the VL-CDR1 consists of the amino acid sequence of SEQ ID NO: 8, the VL-CDR2 consists of the amino acid sequence of SEQ ID NO: 10, and the VL-CDR3 consists of the amino acid sequence of SEQ ID NO: 12. The present invention also provides a method for treating CD24 expressing cancer.

The present specification describes CD24 binding antibodies and their fragments.The antibodies described herein have the useful property of not binding to either B cells or activated T cells.Such antibodies can have an enhanced safety profile with reduced immune side effects.In one aspect, the present specification describes an antibody or its antigen-binding fragment that binds to CD24, and the antibody does not bind to T lymphocytes.In certain embodiments, the antibody does not bind to activated T lymphocytes.