Abstract: In one aspect, provided herein is a method comprising: (a) (i) determining cytolytic activity in a tumor from the subject; and/or (ii) determining genetic alterations associated with cytolytic activity in the tumor; and (b) administering an immunotherapeutic agent to the subject if (i) cytolytic activity is detected in the tumor and/or (ii) a genetic alteration associated with induction of cytolytic activity, tumor resistance to cytolytic activity and/or suppression of cytolytic activity is detected in the tumor.

Abstract: Methods are provided for predicting a response to an anti-PD-1 antibody or anti-PD-L1 antibody therapy based on a new biomarker and for evaluating a malignancy of cancer. The method for predicting a response of a subject to an anti-PD-1 antibody or anti-PD-L1 antibody therapy includes measuring an expression level of LAT1 in a sample collected from a cancer tissue of the subject; and predicting a response of the subject to the anti-PD-1 antibody or anti-PD-L1 antibody therapy based on the expression level of LAT1. The method for evaluating a malignancy of cancer in a subject includes staining a sample collected from a cancer tissue of the subject with an anti-LAT1 antibody and an anti-PD-L1 antibody; and evaluating a malignancy of the cancer in the subject based on a presence or absence of a LAT1-positive and PD-L1-positive site.

Abstract: The present invention relates to a method for the diagnosis or the prognosis of metastasis, relapse or recurrence in prostate cancer which comprises determining if the c-MAF gene is amplified in a primary tumor sample. Likewise, the invention also relates to a method for the diagnosis or the prognosis of metastasis, relapse or recurrence in prostate cancer, as well as to a method for determining the tendency to develop bone metastasis with respect to metastasis in other organs, which comprise determining the c-MAF expression level. Finally, the invention relates to the use of a c-MAF inhibitor as therapeutic target for treating the prostate cancer.

Abstract: The present disclosure relates to one or more agents, therapies, treatments, and methods of use of the agents and/or therapies and/or treatments for selectively inhibiting one or more kinases in one or more tissues. Embodiments of the present disclosure can be used as a therapy or a treatment for a subject where the selective inhibition of kinases with endogenously produced antagonists of kinases may be useful in treating conditions such as cancer, autoimmune disease, and transplant rejection.

Abstract: The present disclosure is directed to methods and compositions for the prediction and treatment of immunotherapy-induced toxicities, as well as improved methods for the treatment of cancer with immunotherapies.

Abstract: The present invention relates to novel liquid pharmaceutical compositions of adalimumab, which include adalimumab or a biosimilar thereof, an acetate buffering agent/system such as sodium acetate/acetic acid, and a sugar stabiliser such as trehalose. Such a combination of components furnishes formulations having a stability (e.g. on storage and when exposed to stress) which is comparable to or an improvement upon those known in the art, and with fewer ingredients. Such advances will help adalimumab treatments to become more widely available at lower cost, and prolong the viability of pre-loaded delivery devices (e.g. pre-filled syringes) to reduce unnecessary waste of the drug.

Abstract: Methods for in vivo immunoimaging including: (a) administering a labeled-antibody conjugate to a subject, wherein the labeled-antibody conjugate includes: an antibody that specifically recognizes and binds to IFN-?, and a detection label conjugated to the antibody, wherein the detection label is a radionuclide tracer or tluorophore; and (b) detecting the presence of the radiolabeled-antibody conjugate in the subject in vivo by imaging. Embodiments of the present disclosure are directed to labeled-antibody conjugates and therapeutic radionuclide-antibody conjugates.

Abstract: Compositions and methods for the treatment of ocular diseases are disclosed. In accordance with one aspect of the instant invention, methods for treating, inhibiting (e.g., reducing), and/or preventing an ocular disease in a subject are provided. The methods comprise the administration of at least one inhibitor of the induction or activity of tryptophan degradation and/or of the downstream pathways that respond to this process. In a particular embodiment, the methods comprise the administration of an inhibitor of IDO1.

Abstract: The present invention relates to novel liquid pharmaceutical compositions of adalimumab, which include adalimumab or a biosimilar thereof, EDTA, and a small polyol stabiliser such as glycerol. Such a combination of components furnishes formulations having a stability (e.g. on storage and when exposed to stress) which is comparable to or an improvement upon those known in the art, and with fewer ingredients. Such advances will help adalimumab treatments to become more widely available at lower cost, and prolong the viability of pre-loaded delivery devices (e.g. pre-filled syringes) to reduce unnecessary waste of the drug.

Abstract: The present invention relates to novel liquid pharmaceutical compositions of adalimumab, which include adalimumab or a biosimilar thereof, arginine and/or methionine, and a small polyol stabiliser such as glycerol. Such a combination of components furnishes formulations having a stability (e.g. on storage and when exposed to stress) which is comparable to or an improvement upon those known in the art, and with fewer ingredients. Such advances will help adalimumab treatments to become more widely available at lower cost, and prolong the viability of pre-loaded delivery devices (e.g. pre-filled syringes) to reduce unnecessary waste of the drug.

Abstract: The present invention provides methods for treating, reducing the severity, or inhibiting the growth of cancer (e.g., skin cancer). The methods of the present invention comprise administering to a subject in need thereof a therapeutically effective amount of a programmed death 1 (PD-1) antagonist (e.g., an anti-PD-1 antibody). In certain embodiments, the skin cancer is cutaneous squamous cell carcinoma or basal cell carcinoma.

Abstract: Yes-associated protein (Yap), a downstream co-activator of the Hippo pathway, is highly expressed in the Treg cell subset, and is critical to maintain its suppressive activity. Originally discovered in Drosophila melanogaster, the Hippo signaling pathway is a major regulator of cellular growth and proliferation in mammals. Loss of Yap expression in Treg cells can lead to superior anti-tumor immune responses, and thus, Yap is an important immunotherapeutic target for cancer.

Abstract: Based on the identification of IL-33 as an exacerbating factor in endometriosis and adenomyosis uteri, a therapeutic agent for endometriosis and adenomyosis uteri has an IL-33 antagonist, which is capable of inhibiting the function of IL-33. The IL-33 antagonist is useful for treating, preventing or alleviating endometriosis and uterine adenomyosis uteri.

Abstract: Antibodies that specifically bind to a Sonic Hedgehog (Shh) polypeptide, or an antigen binding fragment thereof, are provided. Also provided are methods of treating an individual for cancer using the Shh polypeptide antibodies. Methods of analyzing a tissue sample for cell-surface expression of a full-length Shh polypeptide are also provided.

Abstract: Provided herein are formulations of PCSK9-binding polypeptides, such as those comprising evolocumab, that comprise N-acetyl arginine and have reduced viscosities when compared to formulations lacking N-acetyl arginine. Provided herein are also methods of formulating such compositions that are advantageous in that they conserve certain components. Such formulations comprising PCSK9-binding polypeptides can be administered to patients to treat and/or prevent PCSK9-related diseases, conditions, and disorders.

Abstract: Provided herein are methods of treating non-small cell lung cancers comprising administering an effective amount of MEDI4736 or an antigen-binding fragment thereof and tremelimumab or an antigen-binding fragment thereof.

Abstract: Antibody species that bind B-Cell Maturation Antigen (BCMA) are provided as well as methods of depleting BCMA-expressing cells in a patient in need thereof, comprising administering a therapeutically effective amount of the antibody species or an entity comprising a BCMA binding fragment thereof. Methods of treating B cell-related disorders associated with BCMA expression in a patient in need thereof are provided, comprising administering to the patient a therapeutically effective amount of the antibody species or an entity comprising a BCMA binding fragment thereof.

Abstract: Anti-LAG-3 antibodies and antigen-binding fragments thereof are described. Also described are nucleic acids encoding the antibodies, compositions comprising the antibodies, and methods of producing the antibodies and using the antibodies for treating or preventing diseases such as cancer, an inflammatory disease, an autoimmune disease, type 1 diabetes, and/or infectious diseases.

Abstract: A method for selecting an individual to be a candidate for administration of an immune checkpoint inhibitor in treatment of a tumor, comprising: (1) a step of collecting a tumor tissue from the individual, (2) a step of determining the extent of B7-H3 expression in the tumor tissue collected in step (1), and (3) a step of selecting the individual as an individual to be a candidate for administration of the immune checkpoint inhibitor if the B7-H3 expression level is considered to be negative, is provided.

Abstract: This disclosure provides methods for treating a tumor in a subject comprising administering to the subject an anti-PD-1 antibody and an anti-CD30 antibody. In some embodiments, the tumor is derived from a lymphoma (e.g., a Hodgkin lymphoma or a non-Hodgkin lymphoma). In certain embodiments, the anti-CD30 antibody is an antibody-drug conjugate, e.g., brentuximab vedotin.

Abstract: The present invention provides methods for treating, reducing the severity, or inhibiting the growth of cancer (e.g., lung cancer). The methods of the present invention comprise administering a therapeutically effective amount of a programmed death 1 (PD-1) antagonist (e.g., an anti-PD-1 antibody), to a subject with lung cancer wherein the cancer tissue expresses PD-L1.

Abstract: The present invention provides methods for treating moderate-to-severe or severe atopic dermatitis (AD). The methods of the present invention comprise administering to a subject in need thereof one or more doses of an interleukin-4 receptor (IL-4R) inhibitor such as an anti-IL-4R antibody.

Abstract: Disclosed herein is a composition including a recombinant nucleic acid sequence that encodes an antibody. Also disclosed herein is a method of generating a synthetic antibody in a subject by administering the composition to the subject. The disclosure also provides a method of preventing and/or treating disease in a subject using said composition and method of generation.

Abstract: Described is an anti-HSV antibody or an antigen-binding fragment thereof for use in treating an acute infection of mucosal or epidermal tissue in a subject caused by HSV-1 or HSV-2 selected from the group consisting of Herpes simplex labialis, Herpes simplex genitalis, chronic or disseminated cutaneous herpes simplex infection, Herpes gladiatorum and Eczema herpeticum, wherein said antibody is to be topically administered as well as to a pharmaceutical composition comprising an effective amount of said antibody or antigen-binding fragment thereof and at least one pharmaceutically acceptable excipient.

Abstract: The present invention provides methods for treating, reducing the severity, or inhibiting the growth of cancer (e.g., ovarian cancer or pancreatic cancer). The methods of the present invention comprise administering to a subject in need thereof a therapeutically effective amount of an antibody or antigen-binding fragment thereof that specifically binds to programmed death 1 (PD-1) receptor in combination with a therapeutically effective amount of a bispecific antibody that specifically binds Mucin 16 (MUC16) and CD3.

Abstract: The invention provides an improved pan-TGF-? antibody for treatment of conditions that are mediated by TGF-?, including autoimmune diseases, fibrotic conditions, and cancers. Also provided are methods and uses of the antibody in conjunction with other immunomodulatory agents such as an anti-PD-1 antibody.

Abstract: The present invention relates to methods for upregulating immune responses using combinations of anti-RGMb and anti-PD-1 agents.

Abstract: This invention relates methods of using a non-fucosylated anti-CD40 antibody for treatment of cancer and chronic infectious diseases.

Abstract: The present invention provides methods for treating moderate-to-severe or severe atopic dermatitis (AD). The methods of the present invention comprise administering to a subject in need thereof one or more doses of an interleukin-4 receptor (IL-4R) inhibitor such as an anti-IL-4R antibody. In certain embodiments, the methods of the present invention are used to treat severe AD in a patient whose disease is not controlled with systemic therapy (e.g., cyclosporine A) or when such therapy is inadvisable.

Abstract: The present application provides anti-PD-1 antigen-binding proteins or a fragment thereof, as well as nucleic acids encoding anti-PD-1 antigen-binding proteins or CAR T cells expressing such antigen-binding protein or fragment. Also provided are methods of regulating T cells or treating patients using such constructs or cells.

Abstract: The present invention relates to methods of reducing liver PD-1-expressing CD8+ T cells using PD-1 Fc fusion proteins that bind Fc receptors, as well as diagnostic, prognostic, therapeutic methods and compositions related thereto.

Abstract: The present application provides anti-PD-1 antigen-binding proteins or a fragment thereof, as well as nucleic acids encoding anti-PD-1 antigen-binding proteins or CAR T cells expressing such antigen-binding protein or fragment. Also provided are methods of regulating T cells or treating patients using such constructs or cells.

Abstract: The present invention provides methods for treating, preventing or reducing the severity of active eosinophilic esophagitis. In certain embodiments, the present invention provides methods of increasing esophageal distensibility. The methods of the present invention comprise administering to a subject in need thereof a therapeutic composition comprising an interleukin-4/interleukin-13 (IL-4/IL-13) pathway inhibitor such as an anti-IL-4R antibody.

Abstract: The present invention provides a method of assessing whether an individual is at high risk or low risk of inflammatory bowel disease (IBD) progression by determining the expression level of two or more genes in a whole blood sample. Also provided are methods for treating IBD in an individual who is determined to be at high risk or low risk for IBD progression, and kits for assessing whether an individual is at high risk or low risk for IBD progression. Arrays, and methods of providing arrays, of patient-identified selected gene expression products from a whole blood sample of a patient are also provided.

Abstract: Recent large-scale analyses have demonstrated that the genomic landscape of human cancer is complex and variable among individuals of the same tumor type. Such underlying genetic differences may in part be responsible for the varying therapeutic responses observed in cancer patients. To examine the effect of somatic genetic changes in colorectal cancer on sensitivity to a common targeted therapy, we performed complete exome sequence and copy number analyses of 129 tumors that were KRAS wild-type and analyzed their response to anti-EGFR antibody blockade in patient-derived tumorgraft models. In addition to previously identified genes, we detected mutations in ERBB2, EGFR, FGFR1, PDGFRA, and MAP2K1 as potential mechanisms of primary resistance to this therapy. Alterations in the ectodomain of EGFR were identified in patients with acquired resistance to EGFR blockade.

Abstract: Provided is an isolated TrkB agonist antibody that binds to an epitope contained in one of the extracellular domains of TrkB and is capable of activating TrkB, wherein the extracellular domains comprises extracellular D1, D2, D3, D4, D5 domains and juxtamembrane domain of TrkB. Methods of using the TrkB agonist antibody in treating or reducing the risk of a TrkB associated conditions in a subject, wherein said condition is selected from cell differentiation, synaptic development, neural injury repairing and/or neurite branching.

Abstract: The present disclosure provides immunoassay methods of detecting a cleaved high molecular weight kininogen (HMWK) with high sensitivity and specificity and isolated antibodies that specifically bind cleaved HMWK.

Abstract: The present invention relates to a method for the prognosis of bone metastasis in triple negative (including basal-like) breast cancer or, alternatively, ER+ breast cancer (including luminal A and B) which comprises determining if the c-MAF gene is amplified in a primary tumor sample. Likewise, the invention also relates to a method for determining the tendency to develop bone metastasis with respect to metastasis in other organs, which comprise determining the c-MAF gene expression level, amplification or translocation. The invention also relates to a method for predicting early bone metastasis in a subject suffering breast cancer. The invention also relates to a c-MAF inhibitor as therapeutic agent for use in the treatment of triple negative (including basal-like) breast cancer metastasis or, alternatively, ER+ breast cancer (including luminal A and B) metastasis. The invention relates to kits for predicting bone metastasis and predicting the clinical outcome of a subject suffering from bone metastasis.

Abstract: The present invention provides methods, compositions, and combinations for treating cancer via combined use of a compound of formula I or a pharmaceutically acceptable salt, ester, solvate and/or prodrug thereof, wherein A, Q, n, m, R7, R8, V, X1, X2, X3, X4, X5, X6, and X7 are as defined herein, and at least one therapeutically active agents selected from immunotherapeutics, anticancer agents, and anti-angiogenics.

Abstract: The methods, compositions, and assays described herein are based, in part, on the discovery that CD1a mediates inflammation related to certain conditions such as urushiol exposure, psoriasis and other inflammatory skin diseases. One aspect provided herein relates to a method for treating or preventing an inflammatory skin disease, the method comprising: administering a therapeutically effective amount of an inhibitor of CD 1a to a subject having an inflammatory skin disease, thereby treating or preventing the inflammatory skin diseases.

Abstract: The present invention relates to methods of modulating (e.g., reducing) the mannose content, particularly high-mannose content of recombinant glycoproteins.

Abstract: In one aspect, the invention provides methods for treating, inhibiting, alleviating or preventing fibrosis in a mammalian subject suffering, or at risk of developing a disease or disorder caused or exacerbated by fibrosis and/or inflammation. In one embodiment, the invention provides methods of treating a subject suffering from renal fibrosis. In one embodiment, the invention provides methods of reducing proteinuria in a subject suffering from a renal disease or condition associated with proteinuria. The methods comprise the step of administering, to a subject in need thereof, an amount of a MASP-2 inhibitory agent effective to inhibit MASP-2-dependent complement activation.

Abstract: Twenty-one PSGR-derived peptides predicted by an immuno-informatics approach based on the HLA-A2 binding motif were examined for their ability to induce peptide-specific T cell responses in peripheral blood mononuclear cells (PBMCs) obtained from either HLA-A2+ healthy donors or HLA-A2+ prostate cancer patients. The recognition of HLA-A2 positive and PSGR expressing LNCaP cells was also tested. Three peptides, PSGR3, PSGR4 and PSGR14 frequently induced peptide-specific T cell responses in PBMCs from both healthy donors and prostate cancer patients, and are recognized by CD8+ T cells in an HLA-A2 dependent manner. These peptide-specific T cells recognize HLA-A2+ and PSGR+ tumor cells, and killed LNCaP prostate cancer cells in an HLA class I-restricted manner. These PSGR-derived peptides identified are useful as diagnostic markers as well as immune targets for anticancer vaccines.

Abstract: A liposome formulation for delivery of Wnt signal pathway inhibitor is provided herein, which comprises lipid molecules and Wnt signal pathway inhibitor, wherein the liposome formulation is prepared through following steps: (1) providing an aqueous solution of the Wnt signal pathway inhibitor and providing an alcoholic solution of the lipid molecules, (2) mixing the aqueous solution of the Wnt signal pathway inhibitor and the alcoholic solution of the lipid molecules, (3) removing alcohol solvent to obtain the liposome formulation with Wnt signal pathway inhibitor encapsulated therein.

Abstract: A liquid pharmaceutical composition having an anti-TNF? antibody, a buffer, a stabilizer, and a surfactant.

Abstract: Monoclonal antibodies and fragments thereof that are crossreactive with multiple clades of influenza virus including both Group 1 and Group 2 representatives are disclosed. These antibodies are useful in controlling influenza epidemics and pandemics as well as in providing prophylactic or therapeutic protection against seasonal influenza.

Abstract: The present disclosure relates generally to antibodies and functional binding fragments thereof that bind to programmed death-ligand 1 (PD-L1). In particular, the disclosed antibodies and fragments bind to human PD-L1 and comprise novel complementary determining regions (CDRs) also disclosed herein. Finally, the present disclosure relates to administering the disclosed antibodies and fragments to subjects with cancer, thereby treating or slowing the progression or proliferation of the cancer.

Abstract: The invention provides a method for determining whether a human immunodeficiency virus is resistance to a viral entry inhibitor. The methods are particularly useful for determining resistance to inhibitors that act by a non-competitive mechanism. In certain aspects, the methods comprise determining whether an HIV population is resistant to an HIV entry inhibitor, comprising determining a log-sigmoid inhibition curve comprising data points for entry of the HIV population in the presence of varying concentrations of the HIV entry inhibitor, wherein if the entry of the HIV population cannot be completely inhibited by the HIV entry inhibitor, the HIV population is resistant to the HIV entry inhibitor.

Abstract: Compositions and methods for the treatment of ocular diseases are disclosed.

Abstract: The invention relates generally to antibodies that specifically bind programmed cell death protein 1 (PD-1), activatable antibodies that specifically bind to PD-1 and methods of making and using these anti-PD-1 antibodies and anti-PD-1 activatable antibodies in a variety of therapeutic, diagnostic and prophylactic indications.