Resumen de: WO2026030464A1
The disclosure provides methods of dosing for the treatment of cancers, such as multiple myelomas, with anti-fragment crystallizable receptor-like 5 (FcRH5)/anti-cluster of differentiation 3 (CDS) bispecific antibodies (e.g., cevostamab).
Resumen de: WO2026030539A1
Provided herein are mutant anaplastic lymphoma kinase (ALK) nucleic acid molecules and polypeptides, methods related to detecting mutant ALK nucleic acid molecules and polypeptides in cancer, as well as methods of treatment, uses, systems, and non-transitory computer-readable storage media related thereto. A mutant ALK nucleic acid molecule or polypeptide of the present disclosure can be used to identify cancers that are more likely to be resistant to ALK-targeted therapies, or individuals that may benefit from a change in ALK- targeted therapy-based treatment.
Resumen de: WO2026029971A1
Disclosed herein are crystalline polymorphs of indotecan (LMP400) that can be used in the treatment of cancers associated with dysregulation of Topl and/or MYC activity, such as, for example, a sarcoma, (e.g., Ewing's sarcoma), a carcinoma, a hematological cancer, a solid tumor, breast cancer, cervical cancer, gastrointestinal cancer, colorectal cancer, brain cancer, skin cancer, prostate cancer, ovarian cancer, non-small cell lung carcinoma, thyroid cancer, testicular cancer, pancreatic cancer, liver cancer, endometrial cancer, a melanoma, a. glioma, leukemia, a lymphoma, chronic myeloproliferative disorder, myelodysplastic syndrome, myeloproliferative neoplasm, and plasma cell neoplasm (myeloma). This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention.
Resumen de: WO2026029972A1
Disclosed herein are crystalline polymorphs of LMP744 that can be used in the treatment of cancers associated with dysregulation of Top1 and/or MYC activity, such as, for example, a sarcoma, (e.g., Ewing's sarcoma), a carcinoma, a hematological cancer, a solid tumor, breast cancer, cervical cancer, gastrointestinal cancer, colorectal cancer, brain cancer, skin cancer, prostate cancer, ovarian cancer, non-small cell lung carcinoma, thyroid cancer, testicular cancer, pancreatic cancer, liver cancer, endometrial cancer, a melanoma, a glioma, leukemia, a lymphoma, chronic myeloproliferative disorder, myelodysplastic syndrome, myeloproliferative neoplasm, and plasma cell neoplasm (myeloma). This abstract is intended as a scanning tool for purposes of searching m the particular art and is not intended to be limiting of the present invention.
Resumen de: WO2026026715A1
The present application belongs to the field of biomedicine. Disclosed are an siRNA for inhibiting KRAS gene expression, and a modified form thereof and the use thereof. Provided in the present application is a double-stranded RNA molecule targeting KRAS, wherein the molecule can treat KRAS-associated diseases such as metastatic non-small cell lung cancer, metastatic pancreatic ductal adenocarcinoma, KRAS G12C+ non-small cell lung cancer, diabetic retinopathy, leukemia, cholangiocarcinoma, metastatic colorectal cancer, gastric cancer, advanced non-small cell lung cancer, stage-IV non-small cell lung cancer, gastric adenocarcinoma, sepsis, KRAS G12C-mutated advanced non-small cell lung cancer and gallbladder cancer.
Resumen de: WO2026030537A1
Methods of treating relapsed or refractory multiple myeloma by administering (a) a bispecific antibody that binds to CD3 and BCMA. and (b) an anti-CD38 antibody (e.g., daratumumab) to a patient in need are provided.
Resumen de: AU2024296708A1
Methods for treating peripheral T-cell lymphoma include administering to a subject a combination of Cyclophosphamide, Vincristine, Prednisone, and Pralatrexate, wherein the combination does not include doxorubicin. The treatment may be administered in repeated three-week cycles, optionally including a drug holiday.
Resumen de: WO2026025099A1
Compositions and methods for control of DNMT1-mediated site-specific copy gains and genomic insertions associated with mixed lineage leukemia are provided.
Resumen de: WO2026024976A1
The present disclosure relates to methods of treating leukemia using a heterobifunctional molecule, referred to as a cytotoxicity targeting chimera (CyTaC) or antibody recruiting molecule (ARM), that is able to simultaneously bind a target cell-surface protein as well as an exogenous antibody protein.
Resumen de: US20260029402A1
The present study of the regulatory T phenotype of Sézary cells led to the discovery of the expression of GARP (LRRC32) by Sézary cells. GARP has also been shown to be overexpressed in samples from patients with acute lymphoblastic leukemia. GARP therefore appears as a diagnostic marker, for monitoring T-cell malignancies, and as a therapeutic target. Accordingly, the present invention relates to methods for the diagnosis and treatment of T-cell malignancies.
Resumen de: US20260027056A1
The present invention relates to treating malignancies such as tumors or cancers by orally administering lyophilized compositions comprising arsenic to a subject in such need. Malignancies include various hematological malignancies, such as acute myeloid leukemia (AML) including acute promyelocytic leukemia (APL), myelodysplastic syndrome (MDS), multiple myeloma (MM) and lymphomas and solid tumors including glioblastoma multiforme and breast cancer. This invention relates to a novel formulation comprising a lyophilized compositions comprising arsenic. The present invention also relates to a method for lyophilizing the arsenic trioxide, preparing the oral formulation comprising lyophilized compositions comprising arsenic, and a method for treating a subject with malignancies using the oral formulation.
Resumen de: US20260027084A1
The present disclosure provides methods of treating multiple myeloma in a patient in need thereof comprising administering a gamma secretase and a B-cell maturation antigen (BCMA)-directed therapy to the patient.
Resumen de: AU2026200174A1
B-cell maturation antigen (BCMA) is expressed on malignant plasma cells. The present invention provides BCMA-specific chimeric antigen receptors and cells expressing such chimeric antigen receptors. In certain embodiments, engineered cells expressing the chimeric antigen receptors of the present invention are capable of inhibiting the growth of tumors expressing BCMA. The engineered cells of the invention are useful for the treatment of diseases and disorders in which an upregulated or induced BCMA-targeted immune response is desired and/or therapeutically beneficial. For example, engineered cells expressing the BCMA-specific chimeric antigen receptors of the invention are useful for the treatment of various cancers, including multiple myeloma. an a n
Resumen de: AU2024321683A1
Polyfluorinated thalidomide analogs have a structure according to formula I, wherein R is aliphatic. The compounds may be used to inhibit cancer cell proliferation and/or to treat subjects with cancer or an inflammatory process. In some aspects, the cancer is multiple myeloma. In certain aspects, the compounds are used to inhibit proliferation of drug-resistant multiple myeloma cells and/or to treat subjects with drug-resistant multiple myeloma.
Resumen de: WO2026025080A1
This application generally relates to pro-survival complex between a guardian and an effector assembled from their intact BCL-2 globular core domains. In particular, the disclosure relates to methods of identifying modulators of BCL2 antagonist/killer (BAK) binding of Myeloid cell leukemia-1 (MCL-1).
Resumen de: AU2024321532A1
Provided herein are methods for treating a disease or condition selected from the group consisting of cancer, autoimmune disease, graft or transplant-related condition, neurodegenerative disease, fibrotic-associated condition, ischemic-related conditions, infection (viral, parasitic or prokaryotic) and diseases associated with bone loss, the method comprising administering to a patient a therapeutically effective amount of carfilzomib or a pharmaceutically acceptable salt thereof at a dose volume of 10 mL/kg or higher. Also provided herein are methods for treating multiple myeloma in a patient, comprising administering to the patient a pharmaceutical composition comprising carfilzomib or a pharmaceutically acceptable salt thereof and an aqueous carrier, wherein the carfilzomib is administered at a dose volume of 2.5 mL/kg or higher and/or at a concentration of less than 2 mg/mL.
Resumen de: WO2026022712A1
The present disclosure relates to a method of treating cancer (e.g., multiple myeloma) with the combination of i) a multifunctional binding protein comprising a first and a second antigen binding domains (ABDs), wherein the first ABD binds specifically to human BCMA and the second ABD binds specifically to human NKp46; and ii) a cereblon modulating agent.
Resumen de: WO2026024988A1
Methods for treating leukemia are disclosed based on detecting specific cell states and transcriptional programs within leukemic cells. This disclosure presents a novel therapeutic method for treating acute lymphoblastic leukemia (ALL), including BCR-ABL positive and BCR-ABL1-like ALL subtypes. The method involves detecting specific cell states and transcriptional programs in patient samples and administering targeted therapies based on these characteristics. For a pre-B cell-like state or pre-BCR signaling program, a combination of tyrosine kinase inhibitor (TKI) and SYK inhibitor is used. Conversely, a progenitor-like state or stress-autophagy program is treated with a TKI and a p38 MAPK inhibitor. This approach aims to improve treatment efficacy by tailoring therapy to the leukemia's unique molecular and cellular features, particularly in relapsed cases or when minimal residual disease is present.
Resumen de: WO2026025111A1
The present disclosure relates to novel nucleic acids for an immune cell engagers, comprising a ribonucleic acid of formula I: R1 - SP - R2 - R3 - R4 - R5 (I), where R1 is a 5' untranslated region (UTR); SP encodes a signal peptide; R2 encodes a first single chain variable fragment (scFv) that binds a first extracellular protein or a variable region of a heavy chain (VH-only) that binds a first extracellular protein; R3 encodes a second scFv that binds a second extracellular protein; R4 encodes a half-life extender; R5 is a 3'UTR, and where R1 to R5 are oriented 5' to 3', for the treatment of cancers, including but not limited to hematological cancers, including multiple myeloma.
Resumen de: US20260026479A1
The invention relates to genetically engineered mouse models for multiple myeloma (MM) and their uses thereof for the development of multiple myeloma models as well as for the screening of compounds suitable for the treatment of multiple myeloma.
Resumen de: US20260023068A1
The present invention refers to a method for treating Notch signaling-dependent disease in the subject with a FBXO42 specific inhibitor. The Notch signaling-dependent disease is selected from leukemia. Also provided is a method for screening a drug treating Notch signaling-dependent disease using FBXO42 as a target.
Resumen de: AU2024284994A1
Disclosed in the present invention are a CLL1-CAR-T cell, and a preparation method therefor and the use thereof. The CLL1-CAR-T cell contains a chimeric antigen receptor, wherein the chimeric antigen receptor comprises a single domain antibody, a hinge region, a transmembrane region and an intracellular signaling region, and the single domain antibody has an amino acid sequence of positions 22-150 of SEQ ID No. 1. The CLL1-VHH-1 CAR-T cell of the present invention can secrete T cell specific effector molecule IFN-γ to specifically kill CLL1+ target cells, inhibit the proliferation of tumor cells in mice, prolong the survival time of mice, and can be used for immunotherapy of diseases associated with CLL1 target (such as acute myelogenous leukemia).
Resumen de: WO2026020045A1
Aspects of this invention are related to the use of N-desmethyl ruboxistaurin and pharmaceutically acceptable formulations thereof to modulate RSK signaling. Some aspects of the invention relate to the use of N-desmethyl ruboxistaurin to inhibit RSK. Some aspects of the invention provide methods of using N-desmethyl ruboxistaurin in the treatment of subjects with cancer, including breast cancer, ovarian cancer, prostate cancer, lung cancer, hepatocellular carcinoma, colorectal cancer, melanoma, osteosarcoma, myeloproliferative neoplasms, leukemia, and bladder cancer. The disclosed methods extend beyond disease treatment, including supportive care during radiation chemotherapy and prevention of cancer relapse. N-desmethyl ruboxistaurin administration, alone or in combination with other cancer therapies, inhibits RSK and shows a safety profile that supports its long-term use.
Resumen de: AU2024283114A1
Provided are methods for treating CD33-positive hematological malignancies, such as acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS), harboring mutations such as FLT3, IDH1, IDH2, NMP1, and/or MLL1 gene mutations, using combination therapy that includes one or both of a radiolabeled CD33-targeting agent and a drug-conjugated CD33-targeting agent, and one or more targeted therapies, such as FLT3, IDH and Menin inhibitors.
Nº publicación: WO2026017796A1 22/01/2026
Solicitante:
MEDICAL UNIV PLOVDIV [BG]
MEDICAL UNIVERSITY - PLOVDIV
Resumen de: WO2026017796A1
The present invention relates to a system and a method for measuring and analyzing minimal residual disease (MRD) in pediatric B-cell precursor acute lymphoblastic leukemia (B-ALL) using multiparameter flow cytometry (MPFC). The invention finds application in clinical diagnostics and hematology-oncology for quantifying MRD in B-ALL patients with high sensitivity and specificity, needed for risk stratification, monitoring treatment response, and informing therapeutic decisions. The system comprises interconnected subsystems including an acquisition subsystem with an MPFC instrument, a control and file generation subsystem, and an analytical subsystem. The analytical subsystem incorporates modules for sequential data reduction, automated data cleaning, automated unsupervised data clustering, and interactive cluster analysis. Key advantages include high MRD detection sensitivity (e.g., 10⁻⁵ or 0.001%) and high specificity, without reliance on reference samples or supervised machine learning models, making it applicable in laboratories with different measuring equipment and using different panels of antibodies for identification of leukemic cells.