37 results about "Hematologic cancer" patented technology

The present invention relates to methods and compositions for the treatment of BAF-related disorders such as cancer.

Various embodiments of the invention provide binding molecules for B-lymphocyte antigen (e.g., CD 19 and CD20), including antigen recognizing receptors (e.g., CARs) that target B-lymphocyte antigens (e.g., CD 19 and CD20). Embodiments of the invention also provide cells expressing such binding molecules, therapeutics compositions comprising such cells, and methods for treating diseases or disorders associated with B-lymphocyte antigen (e.g., CD19 and CD20), including a hematologic cancer, an autoimmune disease (e.g., multiple sclerosis and systemic lupus erythematosus).

The invention relates to a cucurbituril compound and medical application thereof. Specifically, the invention relates to a compound as shown in a formula (I) and a pharmaceutically acceptable salt thereof, a preparation method thereof, a pharmaceutical composition containing the compound and application thereof as a therapeutic agent, especially application in treatment or prevention of proliferative diseases, cardiovascular related diseases or hematologic cancers, use in reversing drug-induced neuromuscular block and / or anesthesia. I) # imgabs0 #

Provided herein are compositions and methods for treating cancer, e.g., hematological cancer, by administering a CD22 CAR-expressing cell described herein according to a regimen described herein. Also disclosed are methods of making and compositions comprising the same.

The present invention relates to monoclonal humanized antibodies or antigen-binding fragments thereof that specifically bind to the TRBV9 family of human T-cell receptors. The present invention also relates to nucleic acids encoding said antibodies or antigen-binding fragments thereof, expression vectors, methods for preparing said antibodies and the use of said antibodies in the treatment of diseases or disorders associated with said family of human T-cell receptors. The present invention relates to the production of antibodies that can be used to treat, inter alia, ankylosing spondylitis (AS or Bechterev's disease), celiac disease and blood cancers, whose pathogenesis involves T-cell receptors of the TRBV9 family.

Provided herein are compositions and methods for treating a relapsed or refractory hematologic cancer in a human patient in need thereof. The methods entail administering to the patient a daily dose of about 10 mg to about 75 mg of cerdulatinib or a pharmaceutically acceptable salt thereof, wherein the patients suffer one or more of a B-cell malignancy, chronic lymphocytic leukemia (CLL), follicular lymphoma (FL), diffuse large B-cell lymphoma (DLBCL) or other transformed FL and / or have relapsed or not responded to a prior chemotherapy.

Provided herein are small molecule inhibitors for the targeting or IRE1 protein family members. Binding may be direct or indirect. Further provided herein are methods of using IRE1 small molecule inhibitors for use in treating or ameliorating cancer in a subject. Moreover, IRE1 small molecule inhibitors described herein are for the treatment of cancer, where the cancer is a solid or hematologic cancer.

This invention describes CD33 antibodies and their antigen-binding fragments, as well as CD33 / vδ2 multispecific antibodies or their antigen-binding fragments. The invention also describes polynucleotides encoding these antibodies, compositions comprising these antibodies, methods for producing these antibodies, and methods for treating or preventing diseases such as hematological cancers using these antibodies.

The invention relates to multi-specific binding proteins that bind CD19, CD3, and serum albumin. The invention also relates to pharmaceutical compositions comprising these multi-specific binding proteins, expression vectors and host cells for making these multi-specific binding proteins, and methods of use of these multi-specific binding proteins in treating hematologic cancers.

Multiple myeloma (MM) is an incurable hematological cancer, in which immune checkpoint inhibition (ICI) with monoclonal antibodies (mAbs) has failed due to uncontrollable immune responses in combination therapies and lack of efficacy in monotherapies. NK cells have effector activity within the TME, under continuous ligand exposure. NK cell dysfunctionality may occur due to interaction of PD1 and its ligand PD-L1. We created NK cell specific PD1-based chimeric switch receptors (PD1-CSR) by employing signaling domains of DAP10, DAP12 and CD3 to revert NK cell inhibition and retarget ICI. PD1-CSR modified NK cells showed increased degranulation, cytokine secretion and cytotoxicity upon recognition of PDL1+ target cells.

The present invention provides a pharmaceutical formulation comprising negatively charged cyclodextrin or a pharmaceutically acceptable derivative of negatively charged cyclodextrin and a compound # imgabs0 # of formula (I) as specified in the application and the use of these formulations in the treatment of diseases such as cancer. Related compositions, kits, methods of treatment, and methods of manufacture are also provided. The invention is particularly suitable for treating hematologic cancer.

Provided are systems and methods for continuously administering to a subject in need of treatment a formulation comprising an immunomodulatory imide compound. In some embodiments, the method are for use in treating multiple myeloma, transfusion-dependent anemia due to low- or intermediate-1-risk myelodysplastic syndromes, mantle cell lymphoma, hematologic cancers, or solid tumor cancers.

A single domain antibody having binding specificity for the human GPRC5D protein is provided. Such antibodies, and multispecific counterparts and chimeric antigen receptors thereof, are capable of targeting cancer cells expressing GPRC5D, and thus are useful in the treatment of cancer, particularly hematologic cancer.

The present disclosure relates to novel nucleic acids for immune cell adapters, comprising a ribonucleic acid of formula I: R1-SP-R2-R3-R4-R5 (I) wherein R1 is a 5'non-transcriptional region (UTR); sP encodes a signal peptide; r2 encodes a first single chain variable fragment (scFv) that binds to a first extracellular protein or a heavy chain variable region (VH only) that binds to a first extracellular protein; r3 encodes a second scFv that binds to a second extracellular protein; r4 encodes a half-life extender; r < 5 > is 3 'UTR wherein R < 1 > to R < 5 > are in the 5' to 3 'direction for use in the treatment of cancer, including but not limited to hematological cancers, including multiple myeloma.

Disclosed are compositions and methods for targeted treatment of cancer, such as hematologic cancer. In particular, chimeric antigen receptor (CAR) T cells are disclosed that can be used with adoptive cell transfer to target and kill cancer cells with reduced antigen escape. Therefore, also disclosed are methods of providing an anti-tumor immunity in a subject with hematologic cancer that involves adoptive transfer of the disclosed CAR T cells.

This invention discloses 6-substituted 2-([1,1'-biphenyl]-4-yl)quinoline-4-carboxylic acid analogs, which are inhibitors of dihydroorotate dehydrogenase (DHODH) with improved pharmacokinetic properties. The disclosed compounds can be used to treat a variety of disorders and diseases where inhibition of DHODH may be clinically useful, including cancers such as hematologic cancers, including acute myeloid leukemia (AML), graft-versus-host disease, autoimmune disorders, and disorders associated with T-cell proliferation. When administered orally, the disclosed compounds exhibit flipped kinetics, i.e., pharmacokinetics in which the absorption rate, rather than the elimination rate, dominates the pharmacokinetic profile. The disclosed compounds exhibit sustained pharmacokinetic characteristics rather than immediate release characteristics. This summary is intended as a scanning tool for searching in a specific field and is not intended to limit this disclosure.

Provided herein are small molecule inhibitors for the targeting or IRE1 protein family members. Binding may be direct or indirect. Further provided herein are methods of using IRE1 small molecule inhibitors for use in treating or ameliorating cancer in a subject. Moreover, IRE1 small molecule inhibitors described herein are for the treatment of cancer, where the cancer is a solid or hematologic cancer.

The present disclosure is directed to a therapeutic combination of an anti-CD19 antibody and lenalidomide for use in the treatment of hematological cancer patients. Furthermore, the present disclosure concerns extending the overall survival and / or the progression free survival in patients having specific types of hematological cancer.

Methods are provided for treating a hematologic cancer comprising administering an anticancer agent to a subject identified as having an increased mobilization of a subpopulation of lymphocytes from a malignancy following administration of an irreversible Btk inhibitor. Methods also are provided for identification of subjects for treatment and the analysis of cells mobilized from a hematologic malignancy following administration of an irreversible Btk inhibitor.

The present invention relates to methods and compositions for the treatment of BAF-related disorders such as melanoma, prostate cancer, breast cancer, bone cancer, renal cell carcinoma, and hematologic cancer.

PI3Kδ implicates hematologic cancers and solid tumors. Alternative splicing is a post-transcriptional process for acquiring proteomic diversity in eukaryotic cells. Emerging evidence highlights the involvement of aberrant mRNA splicing in cancer development / progression. PI3Kδ-L and PI3Kδ-S are overexpressed in advanced solid tumors, such as prostate, breast, colon, lung and pancreatic cancers. Differential PI3Kδ and PI3Kδ-S expression profiles were identified in a panel of solid tumor cells. PI3Kδ inhibitor Idelalisib and SRPK1 / 2 inhibitor SRPIN340 were employed to assess their efficacies on inhibiting the PI3Kδ-expressing solid tumors. Idelalisib effectively inhibits PI3Kδ-L and its downstream signaling. Idelalisib fails to inhibit PI3Kδ-S activity and its downstream signaling. SRPIN340 reverses the aberrant mRNA splicing, thereby inhibiting the downstream AKT / mTOR signaling. In vitro functional assays further demonstrate that a combination of Idelalisib and SRPIN340 achieve a synergistic drug effect, with drastically reduced cell viabilities / growths of tumor spheroids, in inhibiting the advanced tumor cells.

Methods to inhibit FLT3 activity in a subject or a cell with an FLT3 mutation are provided. Methods of treating a hematologic cancer, such as acute myeloid leukemia, in a subject identified as having an FLT3 mutation, are also provided.

Methods are provided for the continuous administration to a subject requiring treatment of a formulation comprising an immunomodulatory imide compound. In some modalities, the method is used for the treatment of multiple myeloma, transfusion-dependent anemia due to low- or intermediate-risk myelodysplastic syndromes, mantle cell lymphoma, hematologic cancers, or solid tumor cancers.

The invention relates to multi-specific binding proteins that bind CD19, CD3, and serum albumin. The invention also relates to pharmaceutical compositions comprising these multi-specific binding proteins, expression vectors and host cells for making these multi-specific binding proteins, and methods of use of these multi-specific binding proteins in treating hematologic cancers.

Stapled BAD BH3 peptides and compositions comprising the same that are useful in overcoming venetoclax resistance are provided. Also provided are methods of using the stapled BAD BH3 peptides for treating a BCL-2 expressing and / or dependent cancer (e.g., a hematologic cancer or a solid tumor) in a human subject in need thereof. In some cases, the cancer is a venetoclax-resistant cancer due to acquired mutations in the BCL-2 protein. The methods involve administering to the human subject a stapled BAD BH3 peptide or pharmaceutical composition or delivery vehicle comprising the stapled BAD BH3 peptide disclosed herein.

The present disclosure provides a chimeric antigen receptor (CAR) immunotherapy for treating a hematologic cancer comprising (a) genetically modifying a population of immune effector cells comprising T cell receptors (TCRs) to stably express at least one CAR, wherein the ectodomain of the CAR specifically binds a cancer antigen; (b) expanding the population of CAR-containing immune effector cells in the presence of one or more cytokines in vitro to achieve a therapeutic dose, wherein the population of CAR-containing immune effector cells exhibits a nonexhausted memory T cell phenotype; and (c) infusing eligible subjects with the CAR-containing immune effector memory T cell phenotype population of cells as needed until the hematologic cancer in the body is destroyed. The intracellular signal transduction domain of the CAR includes 4-1BB, a CD3zeta T cell activation chain and a genetically engineered 'TLE3, which can be ectopically expressed.

Disclosed are single-chain variable fragments, chimeric antigen receptors, and methods to treat and prevent CD38-associated pathologies, such as hematologic cancers and neurological disorders.

Disclosed herein are compositions comprising a chimeric fusion protein targeting phosphatidylserine on the surface of hematological cancer cells and methods of using the compositions to treat a hematological cancer in a subject.

A method of treating hematological cancer comprising administering to a patient in need thereof a therapeutically effective amount of a phosphatidylinositol 3-kinase gamma (PI3Kg) inhibitor and an antimetabolite, optionally a therapeutically effective amount of a BCL-2 inhibitor. A method of identifying hematological cancer patients susceptible to treatment with a PI3Kg inhibitor. A method of treating hematological cancer, the method comprising administering to a patient in need thereof a therapeutically effective amount of a p-21 activated kinase 1 (PAK-1) inhibitor, optionally a therapeutically effective amount of a BCL-2 inhibitor.

The present disclosure relates to methods of treating hematological cancers, including resistant forms thereof. Also provided are methods of treating aberrantly activated (or reactive) matrices, such as cancer matrices associated with blood system cancers, to alter their state, e.g., to make it / their tolerance to cancer cells low, and / or to reduce the resistance of matrices to treatment with antibodies or antigen-binding fragments thereof, which are inhibitors of the FBG region of tenascin C.