A method of separation of sperm cells with undamaged intact heads from sperm cells with damaged heads and/or somatic cells and/or cell debris in a sperm sample obtained from a human, comprising the steps of: providing an anti-CD46 antibody or CD46-binding ligand bound to a carrier and/or to a tag; contacting the sperm sample with the anti-CD46 antibody or CD46 -binding ligand bound to the carrier and/or to the tag in order to bind CD46 presenting cells and/or cell debris from the sperm sample to the anti-CD46 antibody or CD46-binding ligand; removing the CD46 presenting cells bound via the anti-CD46 antibody or CD46 -binding ligand to the carrier and/or to the tag to obtain a sperm sample free of CD46 presenting cells, wherein CD46 presenting cells include sperm cells with damaged heads, somatic cells and cell debris, is disclosed.

Disclosed are agents for treating or preventing cancers. More particularly, the present invention discloses therapeutic combinations comprising antagonists of receptor of NF-κB (RANK) ligand and immune checkpoint molecules in methods and compositions for treating or inhibiting the development, progression or recurrence of cancers, including metastatic cancers.

The emergence of cells with drug resistant and/or stem cell features might explain frequent relapses and the poor outcome of patients with acute myeloid leukemia (AML). LSCs are heterogeneous for their phenotypes and their sensitivity to chemotherapeutic agents in vivo. Using in silico and functional approaches, the inventors uncovered that CALCRL is overexpressed in LSCs compared with normal hematopoietic cells. They further demonstrated that the CALCRL ligand adrenomedullin (ADM) is highly expressed in AML cells and that increased transcript level was markedly associated with decreased complete remission rates, 5-year overall and event7free survival. The inventors also showed that CALCRL depletion strongly affected leukemic growth in vivo and increased mice survival. Targeting ADM phenocopies the biological and anti-leukemic effects of the CALCRL depletion. These data highlight the critical role of ADM and disclose a promising therapeutic target to specifically eradicate R-LSCs and overcome relapse in AML.

The present invention concerns an anti-sortilin antibody or an antigen binding fragment thereof, for use in the treatment or prevention of a disease of the eye, in particular diseases or disorders of the retina, the choroid and/or the optic nerve.

The present invention concerns an anti-sortilin antibody or an antigen binding fragment thereof, for use in the treatment or prevention of a disease of the eye, in particular diseases or disorders of the retina, the choroid and/or the optic nerve.

Provided are CD3 binding molecules that specifically bind to CD3, for example monospecific binding molecules that specifically bind to CD3 and multispecific binding molecules (MBMs) that specifically bind to CD3 and a tumor-associated antigen, conjugates comprising the CD3 binding molecules, and pharmaceutical compositions comprising the CD3 binding molecules and conjugates. Provided are methods of using the CD3 binding molecules, conjugates, and pharmaceutical compositions to activate T cells in a subject, for example a subject having a cancer or autoimmune disease. Provided are recombinant host cells engineered to express the CD3 binding molecules and methods of producing the CD3 binding molecules by culturing the host cells under conditions in which the CD3 binding molecules are expressed.

The present invention relates to combination therapies useful for the treatment of cancer. In particular, the invention relates to the combined use of a PD-1 inhibitor, a TGFβ inhibitor, an ATM inhibitor and radiation to treat cancer.

Methods and compositions for treating cancer in a subject in need thereof. The method includes administering to the subject an effective amount of a composition comprising Tumor-Targeting Effectors (TITE) derived from a culture comprising a bispecific antibody armed activated T cell (BAT) and a cancer cell, to thereby treat cancer in the subject.

The present invention concerns the combination of CTLA4 and IL-17B inhibitors, especially for the treatment of patients and diseases resistant to anti-CTLA4 therapies.

Provided herein are combinations of an IL-2 molecule or mutein and a TNFR agonist, and complexes comprising IL-2/TNFR agonist molecules, such as Fc-bound IL-2/TNFR agonist molecules that preferentially expand and activate T regulatory cells and are amenable to large scale production. Also provided herein are methods of making and using the compositions of the present invention.