16 results about "Neuropilin" patented technology

The present invention relates to an oligonucleotide comprising from 10 to 25 nucleotides wherein at least one of said nucleotides is modified, and the oligonucleotide hybridizes with the pre-mRNA of the neurociliin 1 (NRP1, CD304) of SEQ ID NO. 366 (GRCh38p13Chr 1033177492-33336262-1) or with the mRNA of the NRP1 of SEQ ID NO. 367 (RefSeq ID NM003873.6). The invention also relates to a pharmaceutical composition comprising the oligonucleotide. The pharmaceutical composition and the oligonucleotide are for use in a method of preventing and / or treating cancer, ophthalmic disease, autoimmune disorder and / or immune disorder.

Provided herein are antibodies, antigen-binding portions thereof, and antibody peptide conjugates that specifically bind to neuropilin-1 (NRP1) and various compositions of such antibodies, antigen-binding portions, and antibody-peptide conjugates. The disclosure also provides nucleic acids encoding the antibodies, antigen-binding portions thereof, or antibody peptide conjugates; cells comprising the nucleic acids; and methods for producing the antibodies, antigen-binding portions thereof, or antibody peptide conjugates. Also provided are methods for using the antibodies or antigen-binding portions thereof in therapeutics and diagnostics for cancer.

Provided are affinity matured and humanized antibodies and antigen-binding fragments thereof that specifically bind to human neuropilin-2 (NRP2) polypeptides, including those that modulate binding interactions between human NRP2 and at least one NRP2 ligand, and which thereby modulate subsequent NRP2-mediated downstream signaling events, including related therapeutic compositions and methods for modulating NRP2 activity and treating diseases such as NRP2-associated diseases.

The present disclosure provides a composition of a degradation agent based on a bispecific binding molecule that degrades a target protein via the lysosomal pathway, such as other proteins on cancer cells other than receptor tyrosine kinase (non-RTK proteins). The bispecific binding molecule specifically binds to a target protein of interest and neuropilin-1 (NRP1). The present disclosure also provides methods of using the bispecific binding molecule-based degrading agents to, for example, enhance the therapeutic efficacy of cancer treatment.

The present invention refers to an oligonucleotide consisting of a core sequence of ATATTTAGGTCCAGCG (SEQ ID NO:1) or AATATTTAGGTCCAGCG (SEQ ID NO:2) and at least one additional nucleotide at the 3´-end and optionally at least one additional nucleotide at the 5´-end. At least one of the nucleotides of the oligonucleotide is modified, and the oligonucleotide binds to pre-mRNA of neuropilin 1 (NRP1, CD304). The invention is further directed to a pharmaceutical composition comprising such oligonucleotide. The pharmaceutical composition and the oligonucleotide are for use in a method of preventing and / or treating cancer, an ophthalmic disease, an autoimmune disorder and / or an immune disorder.

The present disclosure provides a therapeutic method of treating cancer metastasis by inducing clearance of EVs using a binding agent specific to an EV protein. The method utilizes one or more binding agents specific to EV proteins, where the EV proteins are selected from prostaglandin F2 receptor negative regulator (PTGFRN); basigin (BSG); immunoglobulin superfamily member 2 (IGSF2); immunoglobulin superfamily member 3 (IGSF3); immunoglobulin superfamily member 8 (IGSF8); integrin beta-1 (ITGB1); integrin alpha-4 (ITGA4); 4F2 cell-surface antigen heavy chain (SLC3A2); a class of ATP transporter proteins (ATP1A1, ATP1A2, ATP1A3, ATP1A4, ATP1B3, ATP2B1, ATP2B2, ATP2B3, ATP2B4); CD13 (aminopeptidase N); MME (neprilysin), ENPP1 (ectonucleotide pyrophosphatase / phosphodiesterase family member 1); and NRP1 (neuropilin-1). Further provided herein includes a pharmaceutical composition for the treatment of cancer metastasis.

A technology is described which provides a platform for improving the penetration into tumors in a subject of cancer treatment and cancer imaging agents for greater patient benefit. The invention in particular overcomes two challenges for use of tumor targeting methods for solid tumors: poor penetration and the immunosuppressive nature of the tumor microenvironment. The platform described here allows long-term, in vivo production of iRGD. In a preferred embodiment, CAR-T cells are engineered to secrete iRGD, a tumor-penetrating peptide to achieve tissue-penetrating delivery of drugs and imaging agents in a tumor-specific manner. The peptide acutely permeabilizes the tumor vasculature by binding to αv integrins and neuropilin, but in a tumor-specific manner. This method produces a modification in the tumor microenvironment that enhances drug access into the tumor, prevents distant metastasis of the tumor cells, and allows long-term iRGD therapy without the need for repeated injections of iRGD.

This invention relates to a cyclic polypeptide molecular probe targeting neurocilia protein-1 (NRP-1), its preparation method, and its applications. The cyclic polypeptide molecular probe comprises the structure shown in Formula I or Formula II, where R1 is the structure shown in Formula III or Formula IV; and R2 is a radiolabeled nuclide or a radiolabeled nuclide including a bifunctional chelating group. The technical solution of this invention exhibits excellent targeting specificity and high sensitivity for NRP-1 protein, enabling visualization of NRP-1-highly expressing tumors (such as fibrosarcoma, lung cancer, pancreatic cancer, or breast cancer) and NRP-1-positive lesions (such as metabolic diseases, sclerotic lesions, or autoimmune diseases) on positron emission tomography (PET). It shows great promise in the early diagnosis of NRP-1-highly expressing malignant tumors and in guiding clinical NRP-1 monoclonal antibody treatment regimens.

The present invention relates to a cancer therapeutic composition for inhibiting angiogenesis, and a method for preparing the same. The angiogenesis inhibitor according to the present invention is a cancer therapeutic composition containing a fusion protein including a vascular endothelial growth factor binding domain of vascular endothelial growth factor receptor 1 (VEGFR1) and a b1 domain of neuropilin 1 (NRP1). The novel fusion protein is an angiogenesis inhibitor for blocking the binding of VEGF to its receptor on a cell membrane, and has an effect of inhibiting the proliferation of cancer cells as well as the growth and metastasis of cancer. In addition, the fusion protein can be used as an anticancer agent, and exhibits an effective anticancer effect at a lower dose than conventional angiogenesis inhibitors.

The invention relates to the technical field of biomedicine, in particular to a novel target spot for resisting chikungunya virus infection and application. According to the invention, human neuroblastoma cells (SH-SY5Y) and human brain astroblastoma cells (U87) are taken as target cells, and the expression of the target cell part capable of exerting receptor action membrane protein is down-regulated by adopting an RNA interference technology, so that a host factor capable of effectively inhibiting CHIKV infection of human nerve cells is found, and the purpose of blocking CHIKV infection from the source is achieved. The invention discovers that the nerve cilia protein 2 (NRP2) plays an important role in CHIKV infection SH-SY5Y and U87 cells, and the CHIKV infection can be obviously inhibited by down-regulating the expression of the NRP2. The invention provides an application of NRP2 in preparation of a medicine for preventing or treating chikungunya virus infection, and provides a new target spot and a treatment scheme for clinically preventing and treating fever, arthralgia, arthrocele, muscular pain, headache, nausea, fatigue, rash and other diseases caused by CHIKV infection.

The present invention provides methods of treating cancer using antibodies and molecules that bind to BTN1A1 or BTN1A1-ligands. The present invention provides methods of treating cancer using a molecule having an antigen binding fragment that immunospecifically binds to BTN1A1 or a BTN1A1 ligand, such as an anti-BTN1A1 antibody or an anti-BTN1A1 ligand antibody. The present invention also provides a BTN1A1 ligand, such as a galectin-1 (galectin-1), a galectin-9 (galectin-9), a neuropilin-2 (Neuropilin-2), and a B-and T-lymphocyte attenuating protein, for example, a BTN1A1 ligand, for example, a Galectin-1 (Galectin-1), a Galectin-9 (Galectin-9), a Galectin-9 (Galectin-9), a Galectin-2 (

The disclosure provides compositions of a bispecific binding molecule-based degrader that degrades a target protein, such as a protein other than a receptor tyrosine kinase (a non-RTK protein) on a cancer cell, via a lysosomal pathway. The bispecific binding molecule specifically binds to the target protein of interest and to a neuropilin-1 (NRP1). The disclosure also provides methods of using the bispecific binding molecule-based degrader, such as to enhance the therapeutic efficacy of cancer treatment.

The present invention provides methods of treating cancer using antibodies and molecules that bind to BTN1A1 or BTN1A1-ligands. The present invention provides methods of treating cancer using a molecule having an antigen binding fragment that immunospecifically binds to BTN1A1 or a BTN1A1 ligand, such as an anti-BTN1A1 antibody or an anti-BTN1A1 ligand antibody. The present invention also provides a BTN1A1 ligand, such as a galectin-1 (galectin-1), a galectin-9 (galectin-9), a neuropilin-2 (Neuropilin-2), and a B-and T-lymphocyte attenuating protein, for example, a BTN1A1 ligand, for example, a Galectin-1 (Galectin-1), a Galectin-9 (Galectin-9), a Galectin-9 (Galectin-9), a Galectin-2 (

Pancreatic ductal adenocarcinoma (PDAC) has abundant immunosuppressive regulatory T cells (Tregs) which contribute to a tumor microenvironment that is resistant to immunotherapy. Tregs in the PDAC tissue, but not those in the spleen, express the αvβ5 integrin in addition to neuropilin-1 (NRP-1), which makes them susceptible to the iRGD tumor-penetrating peptide that targets αv integrin- and NRP1-positive cells. As a result, long-term treatment of PDAC mice with iRGD leads to a tumor-specific decrease of Tregs and improved efficacy of an immune checkpoint blockade. αvβ5 integrin+ Tregs are induced from both naïve CD4+ T cells and natural Tregs upon T cell receptor stimulation, and represent a highly immunosuppressive subpopulation of CCR8+ Tregs. This study identifies αvβ5 integrin as a marker for activated tumor-resident Tregs that can be expanded to achieve tumor-specific Treg depletion to improve anti-tumor immunity for PDAC management.

Disclosed is a therapeutic agent for treating a cellular immune disease, comprising as an active ingredient a substance that inhibits binding between Sema3A and a Neuropilin-1 / Plexin-A1 heteroreceptor. The substance includes, for example, a Sema3A neutralizing antibody, a Neuropilin-1 neutralizing antibody, or a soluble Neuropilin-1 or derivative thereof. Also disclosed is a method for screening a therapeutic agent for treating a cellular immune disease utilizing a signal generated by the interactions of Neuropilin-1, Plexin-A1 and Sema3A as a marker.

Disclosed are antibodies and fragments thereof that target the A-domain of Neuropilin-1 (Nrp1A). Also disclosed are methods of using the anti-Nrp1A antibodies for the treatment of various diseases or disorders.