Patent classifications
A61K39/464454
Synergistic Inhibition of eIF5A and Notch Signaling
Methods for inducing plasticity in effector T cells to exhibit a regulatory T cell phenotype, treating an autoimmune disease, enriching Treg cells, and preparing a subject for an organ transplant are described. The methods involve the synergstic inhibition of eIF5A and Notch signaling. Also described are compositions and kits including an eIF5A inhibitor and a Notch signaling inhibitor.
Fusion molecule based on TAA variant
This invention provides novel carbonic anhydrase (CAIX) nucleic acid and peptide sequences, as well as related methods and compositions, including anti-cancer immunogenic agent(s) (e.g. vaccines and chimeric molecules) that elicit an immune response specifically directed against cancer cells expressing a CAIX antigenic marker. The novel CAIX variant and related compositions are useful in a wide variety of treatment modalities including, but not limited to protein vaccination, DNA vaccination, and adoptive immunotherapy.
UNIVERSAL CHIMERIC ANTIGEN RECEPTOR T-CELL AND APPLICATION THEREOF
A cell comprising a mutant protein, the mutant protein causing the cell to be insensitive toward an inhibitor which affects the activity and; or killing function thereof; a universal chimeric antigen receptor T cell which is related to the cell and which is suitable for administration to non-specific patients; and a method for preparing the described cells and an application of the cells in cell therapy.
Soluble Mediator
The present disclosure relates to a soluble CD52 glycoprotein and its use in treating diseases regulated by effector T-cells, for example autoimmune diseases such as type 1 diabetes. The present disclosure also relates to fusion proteins comprising the soluble glycoprotein, to cells expressing high levels of CD52, and to diagnostic methods based on the detection of CD52 expression levels in a subject.
Soluble mediator
The present disclosure relates to a soluble CD52 glycoprotein and its use in treating diseases regulated by effector T-cells, for example autoimmune diseases such as type 1 diabetes. The present disclosure also relates to fusion proteins comprising the soluble glycoprotein, to cells expressing high levels of CD52, and to diagnostic methods based on the detection of CD52 expression levels in a subject.
GENETIC EXPRESSION OF HLA MOLECULES TO ENHANCE IMMUNOTHERAPIES
Methods of treating a subject with a tumor, for example in combination with cancer immunotherapy are provided. In some embodiments, the methods include obtaining one or more samples including tumor cells from the subject and measuring human leukocyte antigen (HLA) and/or 2-microglobulin (B2M) expression level, genotype, and/or copy number in the tumor cells. One or more HLA and/or B2M alleles with reduced expression, function, and/or copy number in the tumor are selected and a nucleic acid encoding the one or more HLA and/or B2M alleles is administered to the subject. One or more cancer immunotherapies are also administered to the subject.
GENETIC EXPRESSION OF HLA MOLECULES TO ENHANCE IMMUNOTHERAPIES
Methods of treating a subject with a tumor, for example in combination with cancer immunotherapy are provided. In some embodiments, the methods include obtaining one or more samples including tumor cells from the subject and measuring human leukocyte antigen (HLA) and/or 2-microglobulin (B2M) expression level, genotype, and/or copy number in the tumor cells. One or more HLA and/or B2M alleles with reduced expression, function, and/or copy number in the tumor are selected and a nucleic acid encoding the one or more HLA and/or B2M alleles is administered to the subject. One or more cancer immunotherapies are also administered to the subject.
RADIOIMMUNOTHERAPY DIRECTED TO CCR8 FOR DEPLETION OF TUMOR INFILTRATING REGULATORY T CELLS
Provided are methods for treating a solid cancer in a subject by administering an effective amount of a radioconjugated CCR8-targeting agent to deplete tumor-associated CCR8-positive Treg cells, alone or in combination with one or more additional therapeutic agents or modalities, such as a radioconjugated CD33-targeting agent.
CELL BASED ANTI-CANCER COMPOSITIONS WITH REDUCED TOXICITY AND METHODS OF MAKING THE SAME
Isolated pluralities of T cells which recognize at least one epitope of an intestinal cancer antigen or CNS cancer antigen and pharmaceutical compositions comprising the same are disclosed. Methods of making a plurality of T cells that recognize at least one epitope of an intestinal cancer antigen or CNS cancer antigen are also disclosed. Methods of treating an individual who has been diagnosed with cancer of a mucosal tissue or preventing such cancer in an individual at elevated risk are disclosed as are nucleic acid molecules that comprise a nucleotide sequence that encode proteins that recognize at least one epitope of an intestinal cancer antigen or CNS cancer antigen and T cells comprising such nucleic acid molecules.
FULLY HUMAN ANTIBODY FOR HUMAN B7H3, CHIMERIC ANTIGEN RECEPTOR AND USES THEREOF
Provided are a novel fully human antibody for human B7H3, a chimeric antigen receptor, and uses thereof; also provided are a novel fully human anti-human B7H3 antibody, a chimeric antigen receptor containing the antibody, and genetically engineered cells expressing the receptor and the antibody. It has been verified by experiments that CAR-T, CAR-NK and CAR-iNKT cells targeting B7H3 prepared on the basis of the present chimeric antigen receptor have relatively strong proliferation ability, cytokine release ability and tumor cell killing ability, and can effectively eliminate tumor cells.