The present invention relates to, inter alia, an engineered cell (e.g., iPSC, IPS-derived NK, or NK cell) comprising a disrupted B2M gene and an inserted polynucleotide encoding one or more of SERPINB9, a fusion of IL15 and IL15Rα, and/or HLA-E. The engineered cell can further comprise a disrupted CIITA gene and an inserted polynucleotide encoding a CAR, wherein the CAR can be an anti-BCMA CAR or an anti-CD30 CAR. The engineered cell may further comprise a disrupted ADAM17 gene, a disrupted FAS gene, a disrupted CISH gene, and/or a disrupted REGNASE-1 gene. Methods for producing the engineered cells are also provided, and therapeutic uses of the engineered cells are also described. Guide RNA sequences targeting described target sequences are also described.

The present invention relates to, inter alia, an engineered cell (e.g., iPSC, IPS-derived NK, or NK cell) comprising a disrupted B2M gene and an inserted polynucleotide encoding one or more of SERPINB9, a fusion of IL15 and IL15Rα, and/or HLA-E. The engineered cell can further comprise a disrupted CIITA gene and an inserted polynucleotide encoding a CAR, wherein the CAR can be an anti-BCMA CAR or an anti-CD30 CAR. The engineered cell may further comprise a disrupted ADAM17 gene, a disrupted FAS gene, a disrupted CISH gene, and/or a disrupted REGNASE-1 gene. Methods for producing the engineered cells are also provided, and therapeutic uses of the engineered cells are also described. Guide RNA sequences targeting described target sequences are also described.

The present invention provides antibodies and related molecules that bind to chemokine receptor 4 (CXCR4). The invention further provides antibody-drug conjugates comprising such antibodies, antibody encoding nucleic acids, and methods of obtaining such antibodies. The invention further relates to therapeutic methods for use of these antibodies and anti-CXCR4 antibody-drug conjugates for the treatment of a disorder associated with CXCR4 function or expression (e.g., cancer), such as colon, RCC, esophageal, gastric, head and neck, lung, ovarian, pancreatic cancer or hematological cancers.

The present invention relates to the field of disease therapy. More specifically, it relates to a retargeted herpesvirus having a heterologous polypeptide fused to glycoprotein H, wherein the polypeptide targets diseased cells. It also relates to a nucleic acid comprising the genome of the herpesvirus of the invention, a vector comprising this nucleic acid and a cell comprising the nucleic acid or the vector. It further relates to killing cells using the herpesvirus of the invention and to methods for growing it in vitro.

The present invention relates to the field of disease therapy. More specifically, it relates to a retargeted herpesvirus having a heterologous polypeptide fused to glycoprotein H, wherein the polypeptide targets diseased cells. It also relates to a nucleic acid comprising the genome of the herpesvirus of the invention, a vector comprising this nucleic acid and a cell comprising the nucleic acid or the vector. It further relates to killing cells using the herpesvirus of the invention and to methods for growing it in vitro.

[Problem to be Solved]

To provide a compound for removing pluripotent cells from a cell population potentially containing the pluripotent cells.

[Solution]

A polyphenylalanine derivative is contacted with a cell population of interest.

The present invention provides AAV capsid proteins comprising a modification in the amino acid sequence and virus capsids and virus vectors comprising the modified AAV capsid protein. The invention also provides methods of administering the virus vectors and virus capsids of the invention to a cell or to a subject in vivo.

The present invention provides AAV capsid proteins comprising a modification in the amino acid sequence and virus capsids and virus vectors comprising the modified AAV capsid protein. The invention also provides methods of administering the virus vectors and virus capsids of the invention to a cell or to a subject in vivo.

The present invention relates to a method for inducing the differentiation of corneal epithelial cells from pluripotent stem cells. More specifically, the present invention relates to a method for autonomously differentiating pluripotent stem cells, such as human iPS cells, into ectodermal cell lineage in a serum-free medium without using feeder cells and inducing the differentiation of the resultant ocular surface ectodermal lineage cells into corneal epithelial cells.

The present invention provides EpCAM antibodies with different affinities. The present invention also provides chimeric antigen receptors (CARs) specific to EpCAM. CAR T cells comprising human EpCAM scFv having a low and sufficient affinity to EpCAM can avoid targeting healthy tissues with low EpCAM expression while exhibiting long-term efficacy against tumor tissues with high EpCAM expression. The present invention also relates to an adoptive cell therapy method for treating cancer by administering the CAR-T cells comprising human EpCAM scFv to a subject suffering from cancer, whereby the CAR T cells bind to the cancer cells overexpressing EpCAM and kill the cancer cells.