Abstract: The present invention describes fusion proteins based on cytokines, called bi-cytokines (BC), specifically formed by the binding of an IL2 agonist mutein with a type I interferon (IFN), linked by an Fc region of a mutant human IgG1 and a connector peptide. The combination of an IL2 agonist mutein and a type I IFN in the structure of the bi-cytokines gives surprising immunoregulatory properties to these molecules and a superior therapeutic effect than that of parental cytokines, or their combination, which makes them attractive and novel molecules for the treatment of cancer. Pharmaceutical compositions comprising as an active ingredient the fusion proteins object of this patent are also described.

Abstract: The present invention relates to compositions and methods that provide novel anti-tumor therapies in cancer. In one aspect, the present invention features a hybrid neutrophil in a non-naturally occurring container, wherein the hybrid neutrophil expresses at least one neutrophil associated molecule selected from the group consisting of: Arg1, MPO, CD66b, and CD15, and at least one antigen-presenting cell (APC) associated molecule selected from the group consisting of: CD14, HLA-DR, CD32, CD64, and CD89. In another aspect, the present invention features methods of generating a hybrid neutrophil. In still another aspect, the present invention features methods of inhibiting tumor growth in a subject, treating a tumor in a subject, and increasing efficacy of an antibody against a tumor in a subject. The methods comprise (a) administering to the subject an effective amount of an anti-tumor antibody and (b) administering to or generating in the subject an effective amount of a hybrid neutrophil.

Abstract: The present disclosure provides for antibody-oligonucleotide conjugates, methods of preparation thereof, and methods of use thereof. Also provided are related compounds, compositions and kits.

Abstract: The present invention relates to compounds of formula (I), their enantiomers and their pharmaceutically acceptable salts, and their use in therapy, particularly for the treatment of cancer or inflammatory diseases.

Abstract: Provided are compositions and methods for maintaining intestinal immune homeostasis. The method comprises administering to an individual an effective amount of a VIPR2 inhibitor. The method may modulate gut resident CCR6+ ILC3 cell function.

Abstract: The present invention provides a technique for treating retinal epithelium and/or nerves. More specifically, the present invention is an agent for the treatment or prevention of retinal disease or the like and/or a disease, disorder, or ophthalmological state of the nerves, the agent including at least one factor selected from the group consisting of laminin and fragments thereof, wherein the problem is solved by also providing a technique characterized in that this agent is administered together with retinal pigment epithelial cells and/or nerve cells. Specifically, the present invention can include laminin 411 (?4?1?1), laminin 511 (?5?1?1), laminin 521 (?5?2?1), or fragments of these.

Abstract: Provided herein are novel anti-CD28×anti-B7H3 (also referred to as “?CD28×?B7H3”) heterodimeric bispecific antibodies and methods of using such antibodies for the treatment of cancers. Subject ?CD28×?B7H3 antibodies are capable of agonistically binding to CD28 costimulatory molecules on T cells and targeting to B7H3 on tumor cells. Thus, such antibodies selectively enhance anti-tumor activity at tumor sites while minimizing peripheral toxicity. The subject antibodies provided herein are particularly useful for enhancing anti-tumor activity when used in combination with other anti-cancer therapies.

Abstract: Provided is an antibody targeting CLDN18.2. The antibody targeting CLDN118.2 comprises VL and/or VH; the VL comprises the following CDR sequences: a VL CDR1 amino acid sequence as shown in SEQ ID NO: 11 or SEQ ID NO: 12; a VL CDR2 amino acid sequence as shown in SEQ ID NO: 13; and a VL CDR3 amino acid sequence as shown in SEQ ID NO: 14; and the VH comprises the following CDR sequences; a VH CDR1 amino acid sequence as shown in SEQ ID NO: 15; a VH CDR2 amino acid sequence as shown in SEQ ID NO: 16; and a VH CDR3 amino acid sequence as shown in SEQ ID NO: 17. Further disclosed are a bispecific antibody targeting CLDN18.2, a conjugates of the antibody, a CAR molecule targeting CLDN18.2 and a cell comprising same, and applications thereof.

Abstract: The present disclosure relates to pharmaceutical compositions and methods for treating a disease or condition associated with opening of Cx43 hemichannels in astrocytes or osteocytes, preferably for treating an inflammatory disease or condition or a neurodegenerative disease such as spinal cord injury.

Abstract: The invention relates to a peptide comprising an amino acid sequence selected from the group consisting of (i) SEQ ID NO: 1 to SEQ ID NO: 102, and (ii) a variant sequence thereof which maintains capacity to bind to MHC molecule(s) and/or induce T cells cross-reacting with said variant peptide, or a pharmaceutically acceptable salt thereof.

Abstract: CD38 is expressed on malignant plasma cells. CD28 is a costimulatory molecule required for T-cell activation and survival. Provided herein are novel anti-CD38 antibodies, anti-CD28 antibodies, and bispecific antibodies (bsAbs) that bind to both CD38 and CD28 and act as costimulatory agents to activate T cells via binding CD80 and/or CD86. In certain embodiments, the bispecific antigen-binding molecules of the present invention are capable of inhibiting the growth of tumors expressing CD38. The bispecific antigen-binding molecules of the invention are useful for the treatment of diseases and disorders in which an upregulated or induced CD38-targeted immune response is desired and/or therapeutically beneficial. For example, the bispecific antibodies of the invention are useful for the treatment of various cancers, including multiple myeloma, lymphoma, and leukemia.

Abstract: The present disclosure provides a novel type of drug for treating a subject suffering from an inflammatory and/or autoimmune disease, and specifically rheumatoid arthritis. Specifically, the disclosure provides polypeptides comprising at least three immunoglobulin single variable domains (ISVDs), characterized in that at least one ISVD binds to TNF-? and at least two ISVDs bind to IL-6. The present disclosure also provides nucleic acids, vectors and compositions.

Abstract: Disclosed in the present application are an antibody or an antigen-binding portion thereof binding to human IL-4R, a polynucleotide encoding the antibody or antigen-binding portion thereof, a vector comprising the polynucleotide, a host cell comprising the polynucleotide or vector, a method for preparing and purifying the antibody, and the use of the antibody or antigen-binding portion thereof.

Abstract: As disclosed herein, ?-arrestin1 and ?-arrestin2 levels are highly elevated in brains of FTLD-tau patients suggesting that both ?-arrestin1 and ?-arrestin2 are elevated in the brains of patients with AD and FLTD. The current work also shows that when ?-arrestin2 is overexpressed, tau levels become elevated. The data indicate that ?-arrestin2 reduces tau clearance by impairing p62-mediated autophagy, a role carried out by the oligomerized form of ?-arrestin2. Therefore, disclosed herein are ?-arrestin oligomerization inhibitors that can be used to prevent ?-arrestin oligomerization and therefore the accumulation of tau in cells, i.e. tauopathy. Also disclosed are methods of treating a tauopathy in a subject that involve administering to the subject a therapeutically effective amount of a ?-arrestin oligomerization inhibitor disclosed herein.

Abstract: The invention relates to a peptide comprising an amino acid sequence selected from the group consisting of (i) SEQ ID NO: 1 to SEQ ID NO: 113, and (ii) a variant sequence thereof which maintains capacity to bind to MHC molecule(s) and/or induce T cells cross-reacting with said variant peptide, or a pharmaceutically acceptable salt thereof.

Abstract: Provided is an anti-B7-H3 antibody specifically recognizing a B7-H3, which can be usefully as a cancer therapeutic agent, as having an inhibitory activity of an immune checkpoint which induces antibody-dependent cell-mediated cytotoxicity and T cell activation inhibited by B7-H3. In particular, the antibody having the inhibitory activity of an immune checkpoint can be used in combination with other immunoantibody therapeutic agents. In addition, it can be usefully used for cancer targeting treatment including detection of various cancers expressing B7-H3 through specific binding to B7-H3, and drug delivery to specific cancer, etc.

Abstract: The invention described herein provides antibodies to Zika virus. The novel polypeptides are useful alone or as portions of larger molecules, such as antibodies or antibody fragments, that can be used to treat or prevent infection of Zika virus.

Abstract: Disclosed is a method for producing a modified antibody, comprising: in a heavy chain of the antibody, changing at least one amino acid residue selected from the group consisting of 8th to 11th amino acid residues based on Kabat method to a cysteine residue, and changing at least one amino acid residue selected from the group consisting of 109th and 110th amino acid residues based on IMGT method to a cysteine residue; and recovering the modified antibody.

Abstract: Antibodies to human CD11d, compositions comprising such CD11d antibodies, and methods of using such CD11d antibodies for the treatment of central nervous system trauma including spinal cord injury and traumatic brain injury, as well as systemic inflammatory response following central nervous system trauma.

Abstract: The disclosure relates to means and methods of treating a subject for a CLEC12A positive cancer. In some embodiments the method comprises treating the subject in need thereof with two or more administrations of a bispecific antibody that binds CD3 and CLEC12A, wherein in a first administration an first amount of the bispecific antibody is administered and wherein in each of the subsequent administrations the amount of bispecific antibody is higher than the amount of bispecific antibody in the first administration. In some embodiments CLEC12A positive cancer treatment methods are provided at intervals and dosing regimens that spare hemopoietic stem cell compartment allowing for recovery of normal CLEC12A positive hemopoietic cells.