124 results about "Blocking antibody" patented technology

The present invention provides compositions and methods of use of anti-IGF-1R antibodies or antibody fragments. Preferably the antibodies bind to IGF-1R but not IR; are not agonists for IGF-1R; do not block binding of IGF-1 or IGF-2 to isolated IGF-1R, but effectively neutralize activation of IGF-1R by IGF-1 in intact cells; and block binding of an R1 antibody to IGF-1R. The antibodies may be murine, chimeric, humanized or human R1 antibodies comprising the heavy chain CDR sequences DYYMY (SEQ ID NO:1), YITNYGGSTYYPDTVKG (SEQ ID NO:2) and QSNYDYDGWFAY (SEQ ID NO:3) and the light chain CDR sequences KASQEVGTAVA (SEQ ID NO:4), WASTRHT (SEQ ID NO:5) and QQYSNYPLT (SEQ ID NO:6). Preferably the antibodies bind to an epitope of IGF-1R comprising the first half of the cysteine-rich domain of IGF-1R (residues 151-222). The anti-IGF-1R antibodies may be used for diagnosis or therapy of various diseases such as cancer.

Human breast tumors contain hetrogeneous cancer cells. using an animal xenograft model in which human breast cancer cells were grown in immunocompromised mice we found that only a small minority of breast cancer cells had capacity to form new tumors. The ability to form new tumors was not a slochastic property, rather certain populations of cancer cells were depleted for the ability to form new tumors, while other populations were enriched for the ability to form new tumors. Tumorigenic cells could be distinguished from non-tumorigenic cancer cells based on surface marker expression. We prospectively identified and isolated the tumorigenic cells as CD44³⁰CD24^−/lowLINEAGE A few as 100 cells from this population were able to form tumors the animal xenograft model, while tens of thousands of cells from non-tumorigenic populations failed to form tumors. The tumorigenic cells could be serially passaged, each time generating new tumors containing and expanded numbers of CD44^+CD24 Lineage tumorigenic cells as well as phenotypically mixed populations of non-tumorigenic cancer cells. This is reminiscent of the ability of normal stem cells to self-renew and differentiate. The expression of potential therapeutic targets also differed between the tumorigenic and non-tumorigenic populations. Notch activation promoted the survival of the tumorigenic cells, and a blocking antibody against Notch 4 induced tumorigenic breast cancer cells to undergo apoptosis.

Methods for improved targeting of antibody, antibody fragments, peptides hormones, steroid hormones and conjugates thereof are disclosed. Enhanced delivery to target cells of antibodies or fragments thereof or other receptor-mediated delivery system, such as peptide, specific for a population of cells of a mammal comprises steps of administering to said mammal an adequate dosage of blocking antibodies or fragments thereof or other receptor-mediated delivery system, such as peptide, and administering to said mammal an effective dosage of said antibodies or fragments thereof or other receptor-mediated delivery system, such as peptide, specific for said population of cells. In the preferred embodiment, the specific antibodies are monoclonal antibodies directed toward tumor-associated antigen in man.

Nanosecond pulsed electric field (nsPEF) treatments of a tumor are used to cause the tumor to express calreticulin and stimulate an immune response against the tumor and other tumors in a subject. An immune response biomarker can be measured, and further nsPEF treatments can be performed if needed to stimulate or further stimulate the immune response. Cancers that have metastasized may be treated. The treatment can be combined with CD47-blocking antibodies, doxorubicin, CTLA-4-blocking antibodies, and/or PD-1-blocking antibodies. Electrical characteristics of nsPEF treatments can be based on the size, type, and/or strength of tumors and/or a quantity of tumors in the subject.

The present invention relates to compounds, small interfering RNAs and compositions and methods of inhibiting tumorigenesis and methods of inhibiting tumor cell growth and proliferation using agents that inhibit the hedgehog and Gli signaling pathway, including agents that inhibit GLI synthesis and/or function. The present invention also relates to particular biomarkers that can be used in the diagnosis and prognosis of prostate cancer. Methods of treating cancer, including prostate cancer are also provided using small organic compounds, siRNAs and blocking antibodies that inhibit or block the SHH/GLI pathway.

Methods of treatment to suppress an immune response are provided. The method comprises administering to a subject in need of treatment a naked blocking antibody that binds selectively iNKT cells in an amount effective to suppress the subject's iNKT cell function. Compositions comprising, an isolated, humanized antibody that binds selectively iNKT cells are also provided.

Antibodies are disclosed which bind specifically to P-selectin and which block the binding of PSGL-1 to P-selectin. These anti-P-selectin antibodies may also cause dissociation of preformed P-selectin/PSGL-1 complexes. The disclosure identifies a heretofore unrecognized, near N-terminal, antibody binding domain (a conformational epitope) of P-selectin to which the function-blocking antibodies (which may be chimeric, human or humanized antibodies for example) bind. Antibodies are disclosed which bind to the conformational epitope of P-selectin and which have a dual function in blocking binding of PSGL-1 to P-selectin, and in causing dissociation of preformed P-selectin/PSGL-1 complexes. Such single and dual function anti-P-selectin antibodies and binding fragments thereof may be used in the treatment of a variety of inflammatory and thrombotic disorders and conditions. Screening methods for identifying such antibodies are also disclosed.

The structure, formation and use of blocked antibodies, especially those blocked with Protein A, or active fragments of Protein A, are disclosed as well as processes of producing such antibodies. The uses of such blocked antibodies to achieve significant reduction in both specific cross-reaction and non-specific interaction thereby increasing specificity and reactivity with targeted antigenic sites is also described.

Antibodies are disclosed which bind specifically to P-selectin and which block the binding of PSGL-1 to P-selectin. These anti-P-selectin antibodies may also cause dissociation of preformed P-selectin/PSGL-1 complexes. The disclosure identifies a heretofore unrecognized, near N-terminal, antibody binding domain (a conformational epitope) of P-selectin to which the function-blocking antibodies (which may be chimeric, human or humanized antibodies for example) bind. Antibodies are disclosed which bind to the conformational epitope of P-selectin and which have a dual function in blocking binding of PSGL-1 to P-selectin, and in causing dissociation of preformed P-selectin/PSGL-1 complexes. Such single and dual function anti-P-selectin antibodies and binding fragments thereof may be used in the treatment of a variety of inflammatory and thrombotic disorders and conditions. Screening methods for identifying such antibodies are also disclosed.

Biomarkers are described for predicting the efficacy, risk of relapse, risk of an immune related adverse event (irAE), or combination thereof for a CTLA-4 blockade treatment, such as ipilimumab, in a subject with melanoma. Biomarkers are also described for predicting the efficacy and clinical benefit for a PD-1 blockade treatment, such as a PD-1 blocking antibody, in a subject with melanoma.

The invention discloses an indirect blocking ELISA (Enzyme-Linked Immuno Sorbent Assay) detection kit of an antibody of porcine torque teno virus type II, which comprises an antibody detecting board, an enzyme conjugate working solution, a sample diluent, a coloration solution A, a coloration solution B, a termination solution, a blocking antibody and a washing buffer solution, wherein the blocking antibody is a polyclonal antibody which is obtained in rabbits after purified TTV2 (Torque Teno Virus type II) -ORF1 (Open Reading Frame1) gene antigen epitope area protein immunizes the rabbits. The kit has the beneficial effects of strong specificity and simpleness in operation, is suitable for large-scale clinical popularization and application, and has a good market prospect.

This invention relates, e.g., to methods for inhibiting or stimulating an activity of an adrenomedullin (AM) or gastrin releasing peptide (GRP) peptide hormone, comprising contacting the peptide with a small molecule, non-peptide, modulatory agent of the invention. Complexes of these modulatory agents with other components, such as the peptides or blocking antibodies specific for the peptides, are also described, as are pharmaceutical compositions comprising the modulatory agents, and methods for using the modulatory agents to diagnose or treat patients.

The invention discloses a pig cytomegalovirus antibody indirect blocking enzyme-linked immuno sorbent assay (ELISA) detection kit, wherein an antibody detection board, enzyme combination working solution, a blocking antibody, sample diluent, cleaning solution, developing solution A, developing solution B and stop solution are arranged in the kit. A detection board of the kit is a detachable 96-hole elisa plate wrapped by pig cytomegalovirus g B dominant antigen epitope area protein recombinant antigens, enzyme combination working solution is goat anti-rabbit antibody marked by horse radish peroxidase, and the blocking antibody is a rabbit anti-pig cytomegalovirus g B dominant antigen epitope area protein polyclonal antibody. The pig cytomegalovirus antibody indirect blocking ELISA detection kit has the advantages of being strong in specificity, high in sensitivity, easy to operate and suitable for clinical large-scale popularization and application and has wide market prospect.

The invention relates to a blocking ELISA antibody detection kit for porcinecircovirus type 2 and a preparation method of the blocking ELISA antibody detection kit. The blocking ELISA antibody detection kit for the porcinecircovirus type 2 comprises a coated plate, a PVC2 enzyme labelled antibody, sample diluent, a concentrated washing solution (10*), a positive serum contrast, a negative serum contrast, TMB substrate diluent and a stop solution, wherein the coated plate is prepared from a purified porcine circovirus type 2 nucleocapsid protein CapC protein serving as a non-antigen, and the PVC2 enzyme labelled antibody is prepared from monoclonal antibody hybridoma which is labeled with horse radish peroxidase and secretes PCV2. According to the preparation method, the CapC protein is expressed by virtue of a prokaryotic expression system, and the blocking ELISA is established by taking a monoclonal antibody of PCV2 as the enzyme labelled antibody; and the blocking ELISA antibody detection kit has the characteristics of high specificity and sensitivity and can be applied to the detection of PCV2 antibodies of a porcine serum sample.

The invention discloses a CD 3 and PRLR duplex-specific antibody and construction and application thereof. A construction method of the CD 3 and PRLR duplex-specific antibody comprises the steps thatheavy and light chain plasmids pM-CD3Hc, pM-CD3Lc and pM-IntCRc of a target CD 3 antibody fusion protein IntC are constructed, subjected to transient cotransfection to be transferred into a cell and subjected to affinity purification, and thus a fragment A antibody is obtained; heavy and light chain plasmids pM-PRLRIntN and pM-PRLRLc of a target PRLR antibody fusion protein IntN are constructed, subjected to transient cotransfection to be transferred into the cell and subjected to affinity purification, and thus a fragment B antibody is obtained; the fragment A antibody and the fragment B antibody are subjected to external trans-splicing, and thus the CD 3 and PRLR duplex-specific antibody is obtained. The CD 3 and PRLR duplex-specific antibody provides a new target therapy strategy for current breast cancer HER 2 and ER target treatment; compared with a PRLR blocking antibody, the PRLR-DbsAb has a more obvious inhibiting effect on tumours.

The described invention relates to a pharmaceutical composition comprising a therapeutically effect amount of a therapeutic agent, wherein the therapeutic agent is effective (1) to reduce tumor growth, migration, invasion or a combination and (2) improve subject survival relative to a control. The described invention also relates to a method of treating a subject with a tumor, the method comprising: (1) providing a pharmaceutical composition; and (2) administering the pharmaceutical composition, wherein the composition comprises a therapeutically effective amount of a therapeutic agent which is effective to reduce tumor growth, migration, invasion or a combination. The method may further comprise preparing therapeutic agent and preparing the pharmaceutical composition. The therapeutic agents include but are not limited to Wnt5a derivative peptides or Wnt5a antagonists or Wnt5a blocking antibody. The tumor comprises a population of cancer stem cells.

The invention provides an antitumor preparation and a preparation method for the same. The antitumor preparation is an injection and is in the form of a hydrogel which is formed from an alginate water solution in which active components including a PD-1 blocking antibody and celecoxib are dispersed. The antitumor preparation has excellent in-vivo stability and prolonged sustained-release effect, has significantly improved inhibition effects on growth and migration of tumor cells, and has enlarged anti-tumor spectrum.