Resumen de: WO2026198804A1
Disclosed herein are methods of treating, preventing or ameliorating a disease or condition associated with cancer or a tumor. Some embodiments relate to methods of treating, preventing, or ameliorating relapsed or refractory classical Hodgkin's lymphoma in a subject. In some embodiments, the method includes administering plinabulin to a subject in need thereof, wherein the Hodgkin's lymphoma has progressed following autologous or allogeneic stem cell transplantation and has demonstrated resistance to one or more immune checkpoint inhibitors. In certain embodiments, the method further includes co-administering an immune checkpoint inhibitor, such as a PD-1 or PD-L1 inhibitor, and optionally radiation therapy or a chemotherapeutic agent. In some embodiments, the disclosed methods result in re-sensitization to immune checkpoint inhibitors and provide durable clinical responses in subjects with limited remaining treatment options.
Resumen de: WO2026195138A1
The inventions relate to the field of medicine and pharmaceutics, and more particularly to new protein kinase B inhibitor compounds and methods of producing and using same to treat myeloid leukemia and/or myelodysplastic syndrome. The inventions provide for the clinical effectiveness of immune pathway inhibitors, improved immune control, and suppression of the expression of a number of immune checkpoint molecules, including PD-1L, TIM-3, TIGIT, CD155, CD200 and VISTA, simultaneously on the surface of leukemia cells, which creates the prerequisites for an increase in the rate and duration of remission and an increase in patient survival rates. Through the development of intracellular signalling pathway inhibitors which have the pharmacological effect of suppressing the expression of a number of immune checkpoint molecules on the surface of tumour cells, the inventions widen the range of agents that can be used for treating myeloid leukemia and myelodysplastic syndromes.
Resumen de: US20260285973A1
0000 The present technology aims at providing a novel type of drug for treating a subject suffering from acute myeloid leukemia (AML). Specifically, the present technology provides polypeptides comprising at least three immunoglobulin single variable domains (ISVDs), characterized in that at least one ISVDs binds to T cell receptor αβ (TCRαβ), at least ISVD binds to CD33, and at least one ISVD binds to CD123. The present technology also provides nucleic acids, vectors and compositions.
Resumen de: US20260285879A1
0000 Provided is compound A or a pharmaceutically acceptable salt thereof in a crystalline form. The structure of compound A is represented by formula (I) below. Studies have shown that a crystalline form A-1 of the free base of compound A, crystalline form B of a hydrochloride salt of compound A and crystalline form C of a benzenesulfonate salt of compound A have certain physical stability and chemical stability. The compound A or the pharmaceutically acceptable salt thereof in a crystalline form can significantly inhibit the proliferation of various cells of tumors such as breast cancer, colorectal cancer, ovarian cancer, melanoma, liver cancer, lung cancer and acute myeloid leukemia; and also has a good inhibitory effect on palbociclib-resistant (including primary drug resistance and acquired drug resistance) breast cancer and liver cancer. Therefore, the compound A or the pharmaceutically acceptable salt thereof in a crystalline form has good clinical application prospects in the treatment of advanced malignant tumors, and provides a new drug choice for the treatment of CDK4/6 inhibitor-resistant tumors.
0000
Resumen de: US20260284212A1
0000 Provided herein are human Cluster of Differentiation 6 (CD6) binding molecules and nucleic acid sequences encoding such molecules. In particular embodiments, provided herein are human CD6 binding molecules (e.g., nanobodies) having a first, and optionally a second, single monomeric variable antibody domain (SMVAD) that comprises certain CDRs, and methods for using such molecules to treat T-cell related diseases (e.g., cancer, such as T-cell lymphoma). In certain embodiments, the SMVAD comprises camelid, human, or humanized framework regions.
Resumen de: US20260286007A1
0000 Aspects of the disclosure provide anti-TMPRSS6 antibodies and methods of using the same for promoting hepcidin expression, and treating iron overload associated conditions, such as hemochromatosis, sickle cell disease, thalassemia, hemolysis, Diamond-Blackfan anemia, myelodysplastic syndrome (MDS), blood transfusion.
Resumen de: US20260284190A1
0000 The present invention relates to the combination of anti-CD3 agent, in particular monoclonal antibody, with immunotherapeutic agents, and its use in oncology, for treating T Cell Acute Lymphoblastic Leukemia (T-ALL). The invention also relates to a pharmaceutical composition comprising said combination and the use of said combination to induce cell death of T-ALL cells.
Resumen de: US20260286305A1
The present invention relates to recombinant CAR-NK cells or CAR T-cells, expressing a CAR binding to the antigen CLEC12A or a functional alternatively spliced transcript variant thereof, wherein at least one immune checkpoint receptor protein, such as, for example NKG2A, CLEC12A, PD-1, TIM-3, TIGIT and/or KIRS, is inactivated. These highly functional immune check-point-inactivated CAR-NK cells or CAR T-cells target cancer-associated antigens or are adapted for a treatment of autoimmune diseases. Furthermore, the present invention relates to a non-virus-based method for producing a CAR-NK cell or CAR T-cell expressing an antigen-targeting chimeric antigen receptor (CAR) and a recombinant CAR-NK cell or CAR T-cell as produced, in particular a CAR-NK cell or CAR T-cell targeting the cancer-associated antigen CLEC12A. The present invention also relates to medical uses of the CAR-NK cell or CAR T-cell. The present invention further relates to a CAR-construct, comprising a modified CD8α or CD28
Resumen de: US20260284185A1
Problem A composition and a method that can be used to induce an immune response to HTLV-1 are required.Solution A lipid complex comprising at least one nucleic acid selected from: a nucleic acid comprising a polynucleotide that encodes an immunogenic fragment of human T-cell leukemia virus 1 (HTLV-1) antigenic Gag protein; a nucleic acid comprising a polynucleotide that encodes an immunogenic fragment of HTLV-1 antigenic Tax protein; and a nucleic acid comprising a polynucleotide that encodes an immunogenic fragment of HTLV-1 antigenic HBZ protein; wherein the at least one nucleic acid is encapsulated in a lipid.
Resumen de: WO2025104669A1
The disclosure provides methods of treating a refractory or relapsed acute myeloid leukemia (AML) in a subject comprising administration of a cell comprising a nucleic acid molecule encoding a chimeric antigen receptor (CAR), wherein the CAR comprises an antibody or antigen-binding fragment thereof that binds IL-1RAP, a transmembrane domain, and an intracellular signaling domain comprising at least a stimulatory domain, wherein prior to administering the cell, the subject is preconditioned with a lymphodepleting chemotherapy (LDC).
Resumen de: WO2021158779A1
The present invention includes a method and kit of determining that a patient negative for anti- Ro autoantibodies has Sjögren's syndrome (SS) without performing a lip biopsy comprising: obtaining a liquid biological sample from the patient suspected of having SS; determining that the patient is negative for anti-Ro autoantibodies; and detecting autoantibodies to 1, 2, 3, 4, 5, 6, 7, 8, or 9 proteins selected from: CCDC155, DDB1, MUM1L1, NFU1, RPS29, SOX5, TCP10, ZNF655, or RPAP3, which indicate(s) that the patient has SS. Also, a lack of certain autoantibodies such as KCNAB1, KCNAB2, or as listed in Table 1, Table 2, or Table 3, and Figures 11 or 16 in Ro neg cases may be used to detect SS.
Resumen de: AU2026223298A1
The present invention includes compositions and methods for treating T cell lymphomas and leukemias. In certain aspects, the compositions and methods include CAR T cells targeting CD2, CD5, or CD7 and modified cells wherein CD2, CD5, or CD7 has been knocked-out. ug u g
Resumen de: WO2026188324A1
Provided herein are inducible artificial microRNA (amiRNA) expression vectors for use in the treatment of cancer. In particular, the amiRNAs may be useful for the treatment of cancers selected from one or more of the following: carcinoma; leukemia; lymphoma; myeloma; and sarcoma. More particularly this invention relates to amiRNA expression vectors that are induced by the presence of cell type specific transcription factors and/or cell specific promoters. Such compositions may be designed for the treatment of a wide variety of cancers.
Resumen de: WO2026192941A1
The present invention provides methods of treating Natural Killer (NK) lymphoma in a patient in need thereof, comprising administering to the immunocompetent patient in need thereof an effective amount of a Salt-inducible kinase (SIK)2 and SIK3 (SIK2/3) inhibitor or a pharmaceutically acceptable salt thereof. The present invention further provides a pharmaceutical composition for the treatment of NK lymphoma, comprising a SIK2/3 inhibitor.
Resumen de: WO2026193392A1
Anti-Epstein Barr Virus (EBV) antibodies are described herein. The antibodies can be used to treat and/or reduce the risk of EBV infection and to treat and/or reduce the risk of complications associated with EBV infection, such as infectious mononucleosis, lymphoproliferative disorders, carcinomas, and smooth muscle tumors.
Resumen de: WO2026192899A1
The disclosure is directed to methods of treating acute lymphoblastic leukemia in a subject in need thereof.
Resumen de: WO2026188341A1
A method for assessing a presence of endometriosis, including: collecting a sample of at least one of peripheral blood serum or menstrual fluid from a subject; measuring or detecting an amount of Synuclein gamma (SNCG) and b-cell Lymphoma 6 (BCL6) in the sample: and assessing the presence of endometriosis in the subject based on the amount of SNCG measured or detected in the sample and the amount of BCL6 measured or detected in the sample.
Resumen de: US20260273060A1
Provided are methods and compositions for use in cancer immunotherapies. In various embodiments, the compositions include functionally enhanced derivative effector cells obtained from directed differentiation of genomically engineered iPSCs. In various embodiments, the derivative cells provided herein have stable and functional genome editing that delivers improved or enhanced therapeutic effects. Also provided are therapeutic compositions and the use thereof comprising the functionally enhanced derivative effector cells alone, or with antibodies or checkpoint inhibitors in combination therapies.
Resumen de: US20260273051A1
The present disclosure relates to combination dosing regimen comprising an anti-KMA antibody, an IMiD/CELMOD and a steroid. Such combinations may be used for the treatment of multiple myeloma.
Resumen de: WO2026193438A1
Anti-Epstein Barr Virus (EBV) antibodies are described herein. The antibodies can be used to treat and/or reduce the risk of EBV infection and to treat and/or reduce the risk of complications associated with EBV infection, such as infectious mononucleosis, lymphoproliferative disorders, carcinomas, and smooth muscle tumors.
Resumen de: WO2026193416A1
The present teachings include compositions, methods of synthesis, and methods of use for an imaging agent that preferentially binds to CD38, including but not limited to a peptide or peptidomimetic ligand radiolabeled for use in PET imaging to identify multiple myeloma, help select treatments for multiple myeloma, monitor relapse in multiple myeloma patients after therapy, and treat multiple myeloma.
Resumen de: US20260273112A1
The present teachings include compositions, methods of synthesis, and methods of use for an imaging agent that preferentially binds to CD38, including but not limited to a peptide or peptidomimetic ligand radiolabeled for use in PET imaging to identify multiple myeloma, help select treatments for multiple myeloma, and monitor relapse in multiple myeloma patients after therapy.
Resumen de: AU2025228042A1
The invention relates to combination and combination therapies, particularly for the treatment of a myeloid malignancy, such as acute myeloid leukemia (AML) or a myelodysplastic syndrome (MDS). The combination therapies include (i) a recombinant binding protein comprising (a) an ankyrin repeat domain specifically binding CD3 and (b) at least one, at least two, or at least three further ankyrin repeat domains, wherein each of the at least one, at least two, or at least three further ankyrin repeat domains specifically binds one tumor-associated antigen, suitably one selected from the group consisting of CD123, CD33 and CD70, and (ii) a Bcl-2 inhibitor, e.g., venetoclax, or a pharmaceutically acceptable salt thereof and/or (iii) a hypomethylating agent, e.g., azacitidine or decitabine.
Resumen de: US20260272945A1
Disclosed herein are heterocyclic compounds that inhibit the binding of menin and MLL or MLL fusion proteins. Also described are specific covalent inhibitors of a menin or menin-MLL interaction. Also disclosed are pharmaceutical compositions that include the compounds described herein. Methods of using the menin or menin-MLL irreversible inhibitors are disclosed, alone or in combination with other therapeutic agents, for the treatment of autoimmune diseases or conditions, heteroimmune diseases or conditions, cancer, including lymphoma, leukemia and other diseases or conditions dependent on menin or menin-MLL interaction.
Nº publicación: WO2026190091A1 17/09/2026
Solicitante:
ZENO THERAPEUTICS PTE LTD [SG]
ZENO THERAPEUTICS PTE. LTD.
Resumen de: WO2026190091A1
The invention relates to a method for the evaluation whether a subject diagnosed with acute myeloid leukemia (AML) will have a negative or positive prognosis based on the level of SRRM2 expression on the cell surface of blast cells of said subject and the use of the level of SRRM2 expression on the cell surface of blast cells as prognosis marker for AML. The invention further relates to medical use of SRRM2-targeting therapies for treating SRRM2-positive AML patiens.