Provided are compositions and methods for reducing off-target toxicity of antibody-drug conjugates (ADCs). The compositions comprise an ADC, and an agent targeted to the drug (payload) that is delivered by or derived from the ADC. The ADC and the agent targeted to the payload may be delivered together or separately in the treatment of various conditions (such as tumors) by ADCs. Examples of agents targeted to payload include antibodies, fragments, or modifications thereof.

In various embodiments methods of distinguishing Crohn's disease from ulcerative colitis are provided. In certain embodiments the methods comprise determining, or causing to be determined, the level of IgG antibodies that bind a malondialdehyde-acetaldehyde adduct (MAA adduct) in a biological sample from a mammal, where an elevated level of said antibodies as compared to the average level found in a mammal with Crohn's disease is an indicator that the mammal has ulcerative colitis rather than Crohn's disease.

The present invention provides an in-vitro method of reducing the efficiency of transducing malignant cells of the blood system of a subject that are not derived from T cells with lentiviral vector particles without reducing the efficiency of transducing T cells in a sample comprising T cells and said malignant cells. A combination of compositions comprising a first composition and a second composition is also disclosed, wherein said first composition comprises i) transduced T cells of a subject, wherein said transduced T cells express a CAR comprising an antigen binding domain, wherein the antigen binding domain of said CAR binds specifically to a tag of a tagged polypeptide, and ii) non-transduced malignant cells of the blood system of said subject, and wherein said second composition comprises said tagged polypeptide, wherein said tagged polypeptide binds specifically to an antigen expressed on the surface of said malignant cells. Alternatively, the transduced T cells of said first composition may comprise a nucleic acid encoding a CAR and an inducible gene expression system, and said second composition may comprise an induction agent inducing said gene system.

Example methods comprise administering an immunogenic vaccine composition to a subject, the immunogenic vaccine composition comprising a glycoconjugate. The method can further comprise, in response to the administration of the immunogenic vaccine composition, inducing production of anti-oligomannose antibodies in the subject and thereby eliciting an immune response to a viral pathogen in the subject.

Example methods comprise administering an immunogenic vaccine composition to a subject, the immunogenic vaccine composition comprising a glycoconjugate. The method can further comprise, in response to the administration of the immunogenic vaccine composition, inducing production of anti-oligomannose antibodies in the subject and thereby eliciting an immune response to a viral pathogen in the subject.

Disclosed herein are an anti-HER2 affibody and a switch molecule including a cotinine-conjugated anti-HER2 affibody. When applied in combination with Cot-sCART, the cotinine-conjugated anti-HER2 affibody reacts with HER2-positive cells to induce immune cell activity, thereby finding advantageous applications as switch molecules in sCART therapeutic agents.

The application provides tri-specific antibody monomers having a N-terminal and a C-terminal, comprising in tandem from the N-terminal to the C-terminal, a first scFv domain at the N-terminal, a Fab domain, a Fc domain, and a second scFv domain at the C-terminal. In one embodiment, the first scFv domain, the Fab domain, and the second scFv domain each has a binding specificity against a different antigen.

Anti-Kv1.3 antibodies (mAbs), particularly mAbs that specifically bind to Kv1.3 with high affinity and/or inhibit Kv1.3 function, are disclosed. The amino acid sequences of the CDRs of the light chains and the heavy chains, as well as consensus sequences for these CDRs, of these anti-Kv1.3 mAbs are provided. Additionally, canonical structures for CDRs in the VH and VL regions of anti-Kv1.3 antibodies are provided. The disclosure also provides nucleic acid molecules encoding the anti-Kv1.3 mAbs, expression vectors, host cells, methods for making the anti-Kv1.3 mAbs, and methods for expressing the anti-Kv1.3 mAbs. Finally, methods of using the anti-Kv1.3 mAbs as therapeutics, such as for preventing or treating an autoimmune disorder, are disclosed.

Anti-Kv1.3 antibodies (mAbs), particularly mAbs that specifically bind to Kv1.3 with high affinity and/or inhibit Kv1.3 function, are disclosed. The amino acid sequences of the CDRs of the light chains and the heavy chains, as well as consensus sequences for these CDRs, of these anti-Kv1.3 mAbs are provided. Additionally, canonical structures for CDRs in the VH and VL regions of anti-Kv1.3 antibodies are provided. The disclosure also provides nucleic acid molecules encoding the anti-Kv1.3 mAbs, expression vectors, host cells, methods for making the anti-Kv1.3 mAbs, and methods for expressing the anti-Kv1.3 mAbs. Finally, methods of using the anti-Kv1.3 mAbs as therapeutics, such as for preventing or treating an autoimmune disorder, are disclosed.

A method of treating cervical cancer in a patient in need is described that includes implanting a fast release implant containing an effective amount of Cis-Pt within a cervical cancer lesion. The implant includes a polymer and a therapeutic load homogenously distributed throughout the polymer. The implant assumes a solid phase at room temperature and assumes a liquid phase at a body temperature of the patient.