17 results about "Antibody Suppression" patented technology

The invention provides antibodies that specifically bind tau. The antibodies inhibit or delay tau-associated pathologies and associated symptomatic deterioration.

To provide cross-species anti-latent TGF-β 1 antibodies which inhibit a protease mediated activation of latent TGF-β 1 without inhibiting integrin mediated activation of latent TGF-β 1.SOLUTION: To obtain the anti-latent TGF-β 1 antibodies of the present invention, anti-latent TGF-β 1 antibodies which inhibit a protease mediated activation of latent TGF-β 1 without inhibiting integrin mediated activation of latent TGF-β 1 are screened, and then humanized, and further optimized. The invention also provides combination therapies comprising an anti-latent TGF-β 1 antibody and one or more immune checkpoint inhibitors, preferably PD-1 axis binding antagonists.SELECTED DRAWING: None

Pharmaceutical compositions and therapeutic methods are provided comprising a single-domain antibody consisting of SEQ ID NO:1 and a pharmaceutically acceptable carrier. The antibody inhibits KRAS GTPase activity and inhibits phosphorylation of STAT3. In certain embodiments, inhibition of KRAS results in decreased phosphorylation of ERK1 / 2. The antibody reduces tumor cell surface PD-L1 expression and reduces VEGF production. The antibody crosses the blood-brain barrier following systemic administration and may exhibit sustained biological activity in vivo. Methods are provided for treating KRAS-mutant cancers, including pancreatic cancer and triple negative breast cancer, and for enhancing anti-tumor immunity through reduction of PD-L1 expression.

The present application relates to anti-complement Cls antibodies and uses thereof. The present disclosure provides antibodies that bind complement Cls protein; and nucleic acid molecules encoding such antibodies. The present disclosure also provides compositions comprising such antibodies, and methods of making and using such antibodies, nucleic acid molecules, and compositions. The present disclosure provides an isolated, humanized monoclonal antibody that inhibits cleavage of complement component G4, wherein the antibody does not inhibit cleavage of complement component C2. In some cases, the antibody inhibits a component of the classical complement pathway, in some cases the classical complement pathway component is Cls. In some cases, the antibody does not inhibit protease activity of Cls.

The invention discloses an ATP hydrolase antibody efficient screening method based on a fluorescent probe, the method comprises two detection schemes of a biochemical system and a cell system, in the biochemical system, the antibody inhibition rate is directly calculated by quantifying the residual amount of ENTPD2 protein after ATP hydrolysis; in a cell system, cells over-expressing ENTPD2 are used for verifying the inhibition function of the antibody on transmembrane enzyme. According to the biochemical system method, antibody purification is not needed, primary screening can be completed only through 5-15 microliters of B cell supernate, the screening accuracy is high (the cell system can be used as an antibody obtained through verification and screening), the result is consistent with the in-vivo drug effect result, the method is suitable for development of anti-ENTPD2 antibody drugs, and the research and development cost is remarkably reduced.

To provide an agent for reducing iron overload in patients having conditions such as beta-thalassaemia and myelodysplastic syndrome (MDS).SOLUTION: Antibodies to enzyme matriptase-2 (MTP-2) are presented. Inhibiting MTP-2 reduces uptake of dietary iron and reduces release of iron from cellular stores in the body. Inhibitors of MTP-2 (such as antibodies to a serine protease domain) can be used to treat iron overload, which is a feature of diseases such as beta-thalassaemia and which otherwise leads to toxic accumulation of iron. Combination of an MTP-2 inhibitor with an activin receptor ligand trap, or with erythropoeitin, provides additional therapeutic effects.SELECTED DRAWING: Figure 1

This invention provides novel human antibodies that bind to human galectin-9, and their therapeutic use in the treatment of cancer. [Solution] Provided are isolated anti-galectin-9 antibodies that bind to epitopes in the glycan recognition domain (CRD) of galectin-9 polypeptides, and methods for using anti-galectin-9 antibodies to inhibit galectin-9-mediated signaling pathways or to eliminate diseased cells expressing galectin-9. Such anti-galectin-9 antibodies may also be used to diagnose and / or treat galectin-9-related diseases, such as autoimmune diseases and solid tumors.

Recent studies indicate that sIL7R is involved in the development of autoimmune diseases. The present invention provides methods and compositions for a novel antibody therapeutic against the soluble isoform of the interleukin 7 receptor (sIL7R), a potent driver of self-destructive immune responses that cause autoimmune diseases including multiple sclerosis, lupus nephritis, type I diabetes, rheumatoid arthritis, systemic lupus erythematosus, and many other autoimmune diseases. The present invention includes antibodies specific for sIL7R that inhibit SIL7R, a driver of autoimmunity, without inhibiting mIL7R, thereby reducing the severity of or preventing autoimmunity without activating immunosuppressive mechanisms.

The invention provides antibody heavy chain constant regions with a hinge region modified to reduce binding to Fcγ receptors. The modification occurs within positions 233-236 by replacement of natural residues by glycine(s) and / or deletion(s). Such modifications can reduce binding of an antibody bearing such a constant region to Fcγ receptors to background levels. The constant regions can be incorporated into any format of antibody or Fc fusion protein. Such antibodies or fusion proteins can be used in methods of treatment, particularly those in which the mechanisms of action of the antibody or Fc fusion protein is not primarily or at all dependent on effector functions, as is the case when an antibody inhibits a receptor-ligand interaction or agonizes a receptor.

Antibodies to the enzyme matriptase-2 (MTP-2) are presented. Inhibiting MTP-2 reduces uptake of dietary iron and reduces the release of iron from cellular stores in the body. Inhibitors of MTP-2 (such as antibodies to the serine protease domain) can be used to treat iron overload, which is a feature of diseases such as beta-thalassaemia and which otherwise leads to toxic accumulation of iron. Combination of an MTP-2 inhibitor with an activin receptor ligand trap, or with erythropoietin, provides additional therapeutic effects.

Methods for treating age-related macular degeneration (AMD) or reducing the risk of developing it in subjects are disclosed. These methods may include selecting subjects who have AMD or are at risk of developing it, and administering to the subjects an effective amount of a drug that inhibits HERV-K. Drugs that inhibit HERV-K include, but are not limited to, antibodies, inhibitory RNA molecules, antiretroviral agents, HERV-K-targeting CRISPR / Cas13 systems, and angiogenins. HERV-K-targeting CRISPR / Cas13 systems are also provided. These methods may also include selecting subjects who have AMD or are at risk of developing it, and administering to the subjects an effective amount of a drug that increases ANG activity.

The present invention relates to the treatment of physiologic iron overload and provides antibodies against the proteolysis 2 (MTP-2). Inhibition of MTP-2 reduces dietary iron uptake and reduces iron release from cellular stores in the body. Inhibitors of MTP-2, such as antibodies against the serine protease domain, are useful in the treatment of iron overload, which is characteristic of diseases such as beta-thalassemia and which would otherwise lead to toxic accumulation of iron. Combinations of MTP-2 inhibitors with activin receptor ligand traps or with erythropoietin provide additional therapeutic effects.

The invention provides antibody heavy chain constant regions with a hinge region modified to reduce binding to Fcγ receptors. The modification occurs within positions 233-236 by replacement of natural residues by glycine(s) and / or deletion(s). Such modifications can reduce binding of an antibody bearing such a constant region to Fcγ receptors to background levels. The constant regions can be incorporated into any format of antibody or Fc fusion protein. Such antibodies or fusion proteins can be used in methods of treatment, particularly those in which the mechanisms of action of the antibody or Fc fusion protein is not primarily or at all dependent on effector functions, as is the case when an antibody inhibits a receptor-ligand interaction or agonizes a receptor.

To provide a medicament for treating cancer in an individual or for delaying progression of cancer.SOLUTION: Provided is a medicament for treating cancer in an individual or for delaying progression of cancer in an individual, the medicament comprising an effective amount of an anti-TIGIT antagonist antibody in combination, wherein the anti-TIGIT antagonist antibody inhibits and / or blocks interaction of TIGIT with CD226 and inhibits interaction of TIGIT with PVR, and the medicament comprises an effective amount of an anti-PD-1 antagonist antibody, wherein the anti-PD-1 antagonist antibody inhibits binding of PD-1 to PD-L1.SELECTED DRAWING: Figure 7A-7C

Antibodies against the protease 2 (MTP-2) are provided. Inhibition of MTP-2 reduces dietary iron uptake and reduces release of iron from cellular stores in the body. Inhibitors of MTP-2, such as antibodies against the serine protease domain, are useful in the treatment of iron overload, which is characteristic of diseases such as beta-thalassemia and would otherwise result in toxic accumulation of iron. Combinations of MTP-2 inhibitors with activin receptor ligand traps or with erythropoietin provide additional therapeutic effects.

The invention relates to the technical field of biological detection, and discloses a target pathogenic bacterium immune antibody detection method based on DNA detection. The method comprises the following steps: acquiring target pathogenic bacterium DNA sequence data and immune antibody protein expression quantity data of a biological sample to be detected; mutation site scanning is carried out on the DNA sequence data of the target pathogenic bacteria, the boundary of a high-frequency mutation region is recognized, and the sequence mutation degree is calculated; periodically fluctuating characteristics of antibody expression quantity data are synchronously extracted, and antibody response intensity indexes are generated; determining an immune escape risk coefficient by analyzing the historical correlation and the change trend collaboration degree of the two; constructing an antibody inhibition trend factor by combining the recent decline slope of the expression quantity of the antibody and the rising rate of the DNA copy number of the target pathogenic bacteria; fusing the coefficient and the factor to generate an adaptive evolution index of the target pathogenic bacteria; dynamically adjusting an antibody affinity detection threshold according to the index change gradient and a preset sensitivity threshold; and screening data based on the adjusted threshold, and outputting an effective neutralizing antibody set.

The present invention relates to an isolated humanized protein binding to human Glycoprotein VI (hGPVI) for treating a GPVI-related condition in a subject in need thereof, wherein said isolated humanized protein is to be administered during at least 2 hours to the subject, preferably during at least 4 to 6 hours.