34 results about "Decoy receptors" patented technology

The invention provides FGFR fusion proteins, methods of making them, and methods of using them to treat proliferative disorders, including cancers and disorders of angiogenesis. The FGFR fusion molecules can be made in CHO cells and may comprise deletion mutations in the extracellular domains of the FGFRs which improve their stability. These fusion proteins inhibit the growth and viability of cancer cells in vitro and in vivo. The combination of the relatively high affinity of these receptors for their ligand FGFs and the demonstrated ability of these decoy receptors to inhibit tumor growth is an indication of the clinical value of the compositions and methods provided herein.

The invention provides monoclonal antibodies against decoy receptor 3 (DcR3), hybridomas producing said antibodies, kits containing said monoclonal antibodies and uses of the hybridomas, antibodies and kits for the detection of DcR3-associated diseases, as well as for the treatment and / or prevention of DcR3-associated diseases.

The invention provides fusion protein of a human interleukin receptor C (IL-17RC). The fusion protein contains a key region where the human IL-17RC is bonded with interleukin 17A(IL-17A) and interleukin 17F(IL-17F)and a human IgG1 Fc segment. The IL-17RC-hFc fusion protein provided by the invention has the capacity of binding the IL-17A and the IL-17F, can inhibit release of inflammatory cytokines and expression of RANKL molecules irritated by the IL-17A and the IL-17F, can be used for treating IL-17 associated autoimmune diseases such as rheumatoid arthritis and the like, and exerts the effects of inhibiting inflammation and antagonizing bone destruction. The IL-17RC-hFc fusion protein can serve as a therapeutic bait receptor and provides a new therapeutic approach and thought for diseases such as rheumatoid arthritis and the like. The IL-17RC-hFc fusion protein is subjected to prokaryotic expression in vitro; and the method is high in expression quantity, high in controllability, relatively low in production cost and easy in large-scale production.

The present disclosure relates to a recombinant adenovirus with improved angiogenesis inhibition activity and a pharmaceutical composition for inhibiting angiogenesis. The recombinant adenovirus includes: (a) an inverted terminal repeat (ITR) nucleotide sequence of an adenovirus; and (b) a nucleotide sequence coding for a chimeric decoy receptor containing (i) an extracellular domain of vascular endothelial growth factor receptor 1 (VEGFR-1) and (ii) an extracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2). The recombinant adenovirus according the present disclosure which expresses the chimeric decoy receptor inhibits angiogenesis very effectively and can be used for gene therapy for various angiogenesis-related diseases. Particularly, the recombinant adenovirus of the present disclosure has superior oncolytic activity.

A TGF-β decoy receptor comprising a TGF-β binding region and a lipid anchor region is disclosed. Also disclosed is a chimeric antigen receptor (CAR) comprising a TGF-β binding region. Also disclosed are compositions comprising, and methods using, the TGF-β decoy receptors and CARs.

The present application describes an isolated nucleic acid molecule encoding a polypeptide capable of synchronously binding VEGF polypeptide and placenta growth factor (PIGF) polypeptide comprising a nucleotide sequence encoding a VEGFR1 component.

Provided herein are compositions and related methods for delivering an IgG-decoy receptor to the CNS. The methods include systemic administration of a bifunctional decoy receptor-BBB receptor antibody fusion antibody comprising a receptor extracellular domain (ECD) covalently linked to an antibody to a receptor expressed on the surface of the blood-brain barrier (BBB receptor). In some embodiments, the compositions described herein are administered to treat a subject suffering from a CNS condition.

The present disclosure relates to methods of treating autoimmune conditions in patients who have genetic alterations in the TNFRSF6B gene, which codes for the decoy receptor 3 protein (DcR3), for example that reduce the expression, secretion, or ligand binding activity of DcR3. For example, in some embodiments, the conditions may be treated with molecules that inhibit the activity of DcR3 ligands such as LIGHT, TL1A, and FasL, such as anti-LIGHT, anti-TL1A, and anti-FasL antibodies, or inhibitors of the non-canonical NF-κB pathway.

A TGF-beta decoy receptor comprising a TGF-beta binding region and a lipid anchor region is disclosed. Also disclosed is a chimeric antigen receptor (CAR) comprising a TGF-beta binding region. Also disclosed are compositions comprising, and methods using, the TGF-beta decoy receptors and CARs.

The present invention relates to a VEGF-Grab protein-drug conjugate and a use thereof and, more particularly, to a conjugate of a fusion protein in which a VEGFR1 domain 2, a VEGFR1 domain 3, and an antibody fragment are connected and a drug, a pharmaceutical composition for prevention or treatment of cancer or angiogenesis-related disease, comprising the conjugate, and a method for prevention ortreatment of cancer or angiogenesis-related disease. Serving as a multi-paratopic VEGF decoy receptor, the conjugate including a VEGF-Grab protein and a drug of the present invention can be used as amulti-purpose platform for treatment of cancer or angiogenesis-related disease.

The invention belongs to the field of biological pharmacy and particularly relates to a mutant of a TRAIL (TNF (tumor necrosis factor)-related apoptosis-inducing ligand) and a pharmaceutical application of the mutant. Due to the fact that a wild type TRAIL can be simultaneously combined with tumor cell membrane surface DR (death receptor)4 and DR5 as well as a DcR (decoy receptor)1 and a DcR2 and can be combined with a soluble receptor OPG (osteoprotegrin) by the aid of very low affinity, but tumor cell apoptosis can be induced only through combination of the wild type TRAIL with the DR4 and the DR5; in order to enhance the anti-tumor activity of the TRAIL, the TRAIL mutant having high affinity with the DR5 is designed and constructed, and the TRAIL mutant is characterized by containing E263G mutation, that is, the 263th Glu is mutated into Gly. SEC-HPLC (size exclusion chromatography-high performance liquid chromatography) analysis indicates that the mutant exists in a form of a tripolymer with activity after the mutant is subjected to soluble expression and purification in E.coli. The affinity of the mutant with the DR5 is remarkably improved, and the anti-tumor activity of the mutant is further remarkably improved.

The present invention relates to tumor necrosis factor (TNF) antagonists and corresponding nucleic acids derived from tumor necrosis factor receptors (TNFRs) and their use in the treatment of inflammatory diseases. These proteins are soluble secreted decoy receptors that bind to TNF and prevent TNF from signaling to cells. In particular, the proteins are mammalian TNFRs that lack exon 7 and which can bind TNF and can act as a TNF antagonist.

The present disclosure generally provides compositions and methods related to the field of immunology. Specifically, disclosed herein are chemokine binding proteins and methods of use thereof.

The present invention relates to a composition for preventing or treating cancer comprising Wnt decoy receptor. The composition of the present invention or the expression product thereof inhibits cancer generation, growth, proliferation and metastasis, and induces apoptosis of cancer cells, by binding to Wnt ligand and blocking ligand-receptor interactions, therefore may be effectively used as an anti-cancer agent.

The invention provides fusion protein of a human interleukin receptor C (IL-17RC). The fusion protein contains a key region where the human IL-17RC is bonded with interleukin 17A(IL-17A) and interleukin 17F(IL-17F)and a human IgG1 Fc segment. The IL-17RC-hFc fusion protein provided by the invention has the capacity of binding the IL-17A and the IL-17F, can inhibit release of inflammatory cytokines and expression of RANKL molecules irritated by the IL-17A and the IL-17F, can be used for treating IL-17 associated autoimmune diseases such as rheumatoid arthritis and the like, and exerts the effects of inhibiting inflammation and antagonizing bone destruction. The IL-17RC-hFc fusion protein can serve as a therapeutic bait receptor and provides a new therapeutic approach and thought for diseases such as rheumatoid arthritis and the like. The IL-17RC-hFc fusion protein is subjected to prokaryotic expression in vitro; and the method is high in expression quantity, high in controllability, relatively low in production cost and easy in large-scale production.

The invention is a "preparation method and application of OPG-HSP70 fusion protein", which belongs to the field of biomedical new technology. The invention provides an osteoprotegerin-heat shock protein 70 (OPG-HSP70) fusion protein drug. The drug targets synovitis, the most important pathological feature of rheumatoid arthritis (RA), accompanied by destruction of cartilage and bone. Through osteoprotegerin (OPG) as a decoy receptor, it can interact with cells expressed by osteoblasts and other cells. Receptor Activator of Nuclear Factor κB Ligand (RANKL) binds, blocks the binding of RANKL to RANK expressed by osteoclasts, thereby inhibiting bone resorption involving osteoclasts; uses the protective polypeptide fragment of heat shock protein (HSP) to inhibit joint inflammation. The invention includes the DNA sequence encoding the fusion protein; the method of producing the fusion protein through recombinant technology; and the biological activity of the fusion protein, etc.

Disclosed herein are glyco-decoy acceptor compositions that sidetrack or inhibit the activity of biosynthetic enzymes participating in synthesis of ligands binding at selectin, galectin and siglecs receptors; methods of their preparation and uses in drug discovery and in treatments of diseases.

The present invention relates to tumor necrosis factor (TNF) antagonists and corresponding nucleic acids derived from tumor necrosis factor receptors (TNFRs) and their use in the treatment of inflammatory diseases. These proteins are soluble secreted decoy receptors that bind to TNF and prevent TNF from signaling to cells. In particular, the proteins are mammalian TNFRs that lack exon 7 and which can bind TNF and can act as a TNF antagonist.