The present invention relates to neutralizing antibodies of the human pituitary adenylate cyclase activating polypeptide type I receptor (PAC1) and pharmaceutical compositions comprising such antibodies. Methods of treating or preventing headache conditions, such as migraine and cluster headache, using the neutralizing antibodies are also described.

The CD40L/Mac-1 interaction is selectively targeted by small peptide inhibitors and/or antibodies and such peptides are used for the specific treatment of inflammation and atherogenesis. In particular, pharmaceutical compositions comprising a polypeptide having the amino acid sequence EQLKKSKTL and antibodies specifically binding to an epitope are disclosed.

A use of prevention or treatment of lung cancer including an antibody specifically recognizing CD66c in lung cancer or its antigen-binding fragment and a chemotherapeutic agent is provided.

Described herein are doppel-targeting molecules useful for inhibiting pathological angiogenesis and treating diseases and conditions associated with pathological angiogenesis, such as tumors, cancers, atherosclerosis, tuberculosis, asthma, pulmonary arterial hypertension (PAH), neoplasms and neoplasm-related conditions, and for detecting doppel expression in a subject. Related compositions and methods also are described.

The present disclosure relates to TSLP binding proteins that interact with particular residues of human full length TSLP, or contact particular regions of human full length TSLP. The invention also includes pharmaceutical compositions and medical uses of these TSLP binding proteins.

The present disclosure provides monoclonal antibodies that bind α-Synuclein. In certain aspects, the antibodies preferentially bind to α-Synuclein fibrils over α-Synuclein monomer. In other aspects, the invention comprises a method of treating α-Synucleopathic disease in a subject, comprising administering any of the antibodies of the invention to the subject. In yet other aspects, the invention comprises methods of detecting α-Synuclein fibrils using any of the antibodies of the invention.

In certain aspects, the present disclosure provides compositions and methods for increasing red blood cell and/or hemoglobin levels in a subject in need thereof. Subjects in need include, for example, subjects having anemia and/or ineffective erythropoiesis as a result of having reduced GATA-1, heat shock factor and/or NFE2 levels as compared to the levels in a reference population.

Provided herein are compositions and methods relating to therapies that combine a conjugated activatable anti-CD 166 antibody that when activated specifically binds to CD 166 and an activatable immune checkpoint inhibitor. Also provided herein are compositions and methods relating to therapies that combine an activatable anti-immune checkpoint antibody that when activated specifically binds to the immune checkpoint and a conjugated activatable antibody, where the immune checkpoint is mammalian PD-1 or mammalian PD-L1.

The present invention relates to the fields of molecular medicine and targeted delivery of therapeutic or diagnostic agents to cells outside the vascular system and into the parenchymal tissue of organs within the body. More specifically, the present invention relates to improved TfR-binding moieties based on shark VNARs capable of crossing the blood brain barrier (BBB) and capable of carrying and releasing cargo specifically targeted to the parenchymal tissue of the brain.

The present disclosure provides antibodies, including antibody fusions, which specifically bind to human CSF1 receptor protein (huCSF1R) and are capable of decreasing, inhibiting, and/or fully-blocking immune regulatory effects mediated by huCSF1R, such as regulation of TAMs in the tumor microenvironment. Additionally, the antibodies include fusions with the cytokine inhibitory factor, IL10, which can replenish and/or activate CD8+ T-cell cytotoxicity in the tumor microenvironment. The present disclosure also provides methods of using the antibodies (and compositions thereof) to treat diseases and conditions responsive to decreasing, inhibiting and/or blocking immune regulatory function or activity mediated by CSF1 binding to CSF1R.