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57
resultados
Última actualización
10/03/2026 [06:45:00]
Resumen de: US20260062458A1
The present invention provides a chimeric antigen receptor (CAR) comprising: (i) a B cell maturation antigen (BCMA)-binding domain which comprises at least part of a proliferation-inducing ligand (APRIL); (ii) a spacer domain (iii) a transmembrane domain; and (iv) an intracellular T cell signaling domain. The invention also provides the use of such a T-cell expressing such a CAR in the treatment of plasma-cell mediated diseases, such as multiple myeloma.
Resumen de: WO2026050126A1
Methods for classifying cancers to aid in diagnosis and treatment of the cancer, in particular acute leukemia and solid tumors such as pediatric sarcomas, in a rapid manner (less than 24 hours). Methods comprising the use of long-read whole genome sequencing of libraries comprising high molecular weight DNA to identify copy number variations and/or presence or absence of a mutation such as a karyotype abnormality or translocation/gene fusion in a panel of targets and treatment of patients based upon cancer classification.
Resumen de: US20260060991A1
Clonal hematopoiesis is an age-related condition caused by somatic mutations that give a hematopoietic stem cell a clonal selective advantage. While clonal hematopoiesis is a benign condition, individuals affected by it have an increased risk of developing blood cancers, such as acute myeloid leukemia (AML). The present disclosure provides, in some aspects, methods for inhibiting clonal hematopoiesis using a senolytic agent to target senescence of bone marrow stromal cells.
Resumen de: US20260060222A1
A mouse with a humanization of the mIL-3 gene and the mGM-CSF gene, a knockout of a mRAG gene, and a knockout of a mIl2rg subunit gene; and optionally a humanization of the TPO gene is described. A RAG/Il2rg KO/hTPO knock-in mouse is described. A mouse engrafted with human hematopoietic stem cells (HSCs) that maintains a human immune cell (HIC) population derived from the HSCs and that is infectable by a human pathogen, e.g., S. typhi or M. tuberculosis is described. A mouse that models a human pathogen infection that is poorly modeled in mice is described, e.g., a mouse that models a human mycobacterial infection, wherein the mouse develops one or more granulomas comprising human immune cells. A mouse that comprises a human hematopoietic malignancy that originates from an early human hematopoietic cells is described, e.g., a myeloid leukemia or a myeloproliferative neoplasia.
Resumen de: US20260060969A1
Inventors have first investigated the impact of PIK3CA inhibition in NZBWF1/J mice a model of lymphoproliferative disorders. They randomly assigned 30 females aged of 24 weeks to receive either vehicle (n=15) or alpelisib (n=15) during 4 weeks. At the time of sacrifice, alpelisib treated mice demonstrated significantly reduced spleen size. Flow cytometry analysis revealed that B cells were significantly reduced in alpelisib treated mice and CD8 cells count corrected. They then decided to explore the relevance of alpelisib in MRL/MpJ-Faslpr/J mice (referred here as MRL-lpr), another mouse model of lymphoproliferative disorder. These mice with homozygous Fas mutation usually develop severe lymphadenoproliferation. At the time of sacrifice. MRL-lpr mice treated with alpelisib demonstrated a reduction on their spleen and lymph node sizes. Flow cytometry analysis showed correction of B cells. T cells and other immune cells in peripheral blood mononuclear cells (PBMC), lymph nodes and spleen. The invention relates to a method for treating lymphoproliferative disorder in a subject in need thereof comprising a step of administering the subject with a therapeutically effective amount of a PIK3CA inhibitor.
Resumen de: AU2024294756A1
Embodiments of the present invention relate to methods of reducing oral toxicities, such as taste impairment, in subjects that undergo treatment with a GPRC5D- targeted therapeutic.
Resumen de: WO2026050255A2
The present disclosure provides monospecific antigen-binding proteins that bind human SLC3A2-APIS and bispecific antigen-binding proteins that bind to SLC3A2-APIS and CDS (SLC3A2-APISxCD3). In certain embodiments, the disclosed bispecific antigen-binding proteins include a first antigen-binding domain that binds SLC3A2-APIS and a second antigen-binding domain that binds CDS. In some embodiments, the disclosed antigen-binding proteins inhibit tumor growth. In some embodiments, the disclosed antigen-binding proteins ameliorate one or more symptoms of a myelodysplastic syndrome.
Resumen de: WO2026047495A1
The present invention provides a computer implemented method for predicting the risk of posttransplant lymphoproliferative disorder as well as a computer implemented method for simultaneous predicting the risk of posttransplant lymphoproliferative disorder and differentiation of Epstein Barr Virus (EBV)-positive from EBV-negative patients in posttransplant lymphoproliferative disorder and associated systems. The method for predicting the risk of posttransplant lymphoproliferative disorder PTLD, comprises the following steps: receiving information representative for expression level of biomarkers, acquired from a sample to be assessed, said biomarkers being at least three selected from the group comprising HSPA6, CD300A, IFITM1, SHFL, HMGB1, TMEM163, ELL3, GRHPR, GMDS, GALNT10, IRF1-AS1, IFIT5, MLLT3, KIR2DL4, CD1C, SP3, SLC6A16, COP1, classifying said information representative for expression level of said at least three biomarkers, outputting the classification results, said results being indicative of whether the assessed sample belongs to one of two classes: PTLD or non-PTLD patient. The present invention provides further biomarkers for predicting, diagnosing and differentiating of posttransplant lymphoproliferative disorders and use thereof.
Resumen de: US20260061029A1
Identification of effective targets alleviating the programmed cell removal (PrCR) of tumor cells by macrophages is of very high interest. The present inventors have identified that the cyclin-dependent kinase inhibitor p21 protein is a strong regulator of the macrophage-mediated PrCR. Also, they showed that the adoptive transfer of p21 overexpressing monocytes induces macrophage PrCR and transition from an anti-inflammatory to a pro-inflammatory phenotype in vivo, delays cancer progression and increases significantly the overall survival of mice engrafted with cancer cells. The present invention therefore concerns therapeutic compositions comprising monocytes that over-express the cyclin-dependent kinase inhibitor p21 protein, and their use for treating mammals suffering from cancer, especially leukemia.
Resumen de: WO2026047608A1
Disclosed herein are differences in the features of immune cell populations in subjects with monoclonal gammopathy of unknown significance (MGUS) or smoldering myeloma (SMM), compared to subjects with multiple myeloma (MM). These features are useful in methods for monitoring progression from MGUS or SMM to MM in a subject. In some instances, certain features are also useful in methods for predicting the response of a subject's MM to therapy.
Resumen de: US20260062760A1
A method of treating multiple myeloma, comprising administering one or more agents increasing or inhibiting the expression or activity of one or more MM biomarkers to inhibit the progression of multiple myeloma, wherein the one or more MM biomarkers correspond to gene products from one or more of GABRA3, CTAG2, MAGEA6, SOHLH1, MAGEA1, AFAP1-AS1; CBX2, LINC00484, KIF7, TMSB15A, NEK2, NTRK1, CCND2, NES, PKP2, C1orf226, IFITM1, CDH23, AGRN, DHX58, and LINC02576. A method of diagnosing and treating multiple myeloma in a subject comprises, (a) measuring the level of one or more biomarkers in a sample; (b) comparing the level of the one or more biomarkers to a reference level of the one or more biomarkers; (c) making a diagnosis based on the result of the comparing step; and (d) treating the subject with one or more active agents where the subject is diagnosed with multiple myeloma.
Resumen de: US20260062417A1
Described herein is the Bruton's tyrosine kinase (Btk) inhibitor 1-((R)-3-(4-amino-3-(4-phenoxyphenyl)-1H-pyrazolo3,4-dpyrimidin-1-yl)piperidin-1-yl)prop-2-en-1-one, including crystalline forms, solvates and pharmaceutically acceptable salts thereof. Also disclosed are pharmaceutical compositions that include the Btk inhibitor, as well as methods of using the Btk inhibitor, alone or in combination with other therapeutic agents, for the treatment of autoimmune diseases or conditions, heteroimmune diseases or conditions, cancer, including lymphoma, and inflammatory diseases or conditions.
Resumen de: AU2026200996A1
Discussed herein are pharmaceutical compositions containing Ibrutinib and processes for preparing them. The compositions may be utilized in the treatment of a variety of conditions including, without limitation, B-cell proliferative disorders such as non-Hodgkin lymphoma (diffuse large B cell lymphoma, follicular lymphoma, mantle cell lymphoma or burkitt lymphoma), Waldenstrom macroglobulinemia, plasma cell myeloma, chronic lymphocytic leukemia, lymphoma, or leukemia. These compositions are designed for oral ingestion. The compositions are contained within a capsule such as a standard or sprinkle or in a liquid formulation such as a suspension. In one embodiment, the pharmaceutical composition contains Ibrutinib, a salt, prodrug, or metabolite thereof, microcrystalline cellulose, croscarmellose sodium, sodium lauryl sulfate, and magnesium stearate. In another embodiment, the pharmaceutical composition contains Ibrutinib, a salt, prodrug, or metabolite thereof, microcrystalline cellulose, carboxymethylcellulose sodium, hydroxypropylmethylcellulose, citric acid monohydrate, disodium hydrogen phosphate, sucralose, sodium methyl parahydroxybenzoate, sodium ethyl parahydroxybenzoate, concentrated hydrochloric acid, sodium hydroxide, and water. eb e b
Resumen de: WO2026050474A1
The present invention relates to the treatment of subjects having a CD20-positive cell proliferative disorder (e.g., B cell proliferative disorders, such as a non-Hodgkin's lymphoma (NHL); e.g., an aggressive NHL or a relapsed and/or refractory NHL). More specifically, the invention pertains to the treatment of subjects having a B cell proliferative disorder by administering a combination of mosunetuzumab and polatuzumab vedotin.
Resumen de: HRP20251441A1
Provided herein are methods of treating a subject who has multiple myeloma and has received one to three prior treatment(s). Infusions of chimeric antigen receptor (CAR)-T cells comprising a CAR capable of specifically binding to an epitope of BCMA are administered to the subject.
Resumen de: WO2026044177A1
Herein are methods of treating multiple myeloma in a subject comprising administering GPRC5D antibodies with enhanced antibody-dependent cellular cytotoxicity (ADCC) and enhanced complement-dependent cytotoxicity (CDC). The antibodies described in the methods are afucosylated and comprise K248E and T437R mutations (designated as "RE mutations") per the EU numbering system.
Resumen de: WO2026042913A1
The objective of the present invention is to treat cancer in affected dogs by using interleukin-15, which plays a pivotal role in both innate immunity and acquired immunity. Specifically, the present invention relates to a composition for treating cancer in mammary tumor- or lymphoma-affected dogs, or an anticancer immune enhancer, comprising recombinant canine interleukin-15. The present invention also relates to the dosage and use of recombinant canine interleukin-15 in the treatment of cancer in mammary tumor- or lymphoma-affected dogs. The present invention can exhibit therapeutically effective anticancer- or anticancer immunity-enhancing efficacy by minimizing harmful effects or side effects after standard treatment in mammary tumor- or lymphoma-affected dogs by using recombinant canine interleukin-15.
Resumen de: US20260053939A1
This disclosure provides combination therapies comprising an anti-BCMA antigen binding protein, such as belantamab mafodotin; an immunomodulatory imide drug (IMiD); a proteasome inhibitor; and a corticosteroid. This disclosure also provides combination therapies for treating newly diagnosed multiple myeloma.
Resumen de: US20260055203A1
The present invention relates to the treatment of subjects having CD20-positive cell proliferative disorders (e.g., B cell proliferative disorders, such as non-Hodgkin's lymphomas). More specifically, the invention pertains to the treatment of subjects having a B cell proliferative disorder by intravenous administration of an anti-CD20/anti-CD3 bispecific antibody (e.g., mosunetuzumab).
Resumen de: US20260055202A1
The present disclosure provides multiple anti-hCD20 mAbs as well as humanization of antibodies. The antibodies described herein are chicken-derived and exhibit significantly enhanced B-cell-specific antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) potency as well as improved depletion of B lymphoma cells in vivo relative to Rituximab.
Resumen de: WO2026040955A1
The present application discloses a pharmaceutical combination comprising a bispecific anti-CD3/CD20 polypeptide complex and a second therapeutic agent, and use thereof in the preparation of a drug for treating non-Hodgkin lymphoma.
Resumen de: WO2026042623A1
Provided is a method for diagnosing the prognosis and therapeutic effect for chemotherapy in patients with rheumatoid arthritis-associated lymphoproliferative disorder (RA-LPD), who have developed a lymphoproliferative disorder (LPD) during the treatment of rheumatoid arthritis (RA). This is a kit for diagnosing the prognosis and therapeutic effect for chemotherapy in rheumatic arthritis-associated lymphoproliferative disorder (RA-LPD) patients, who have developed LPD during RA treatment. The kit comprises: means for detecting an inositol 1,4,5-triphosphate receptor (ITPR) type 2 (ITPR2) gene mutation in a biological sample from a patient; and instructions for determining that the prognosis and therapeutic effect for chemotherapy are poor when an ITPR2 gene mutation is present in the biological sample from the patient. The LPD is diffuse large B-cell lymphoma (DLBCL). For the ITPR2 gene mutation, Chr12:rs26744460 is GT or GG. Use for the diagnosis of non-RA lymphoma patients is also possible.
Resumen de: US20260055473A1
A method of treating multiple myeloma, comprising administering one or more agents increasing or inhibiting the expression or activity of one or more MM biomarkers to inhibit the progression of multiple myeloma, wherein the one or more MM biomarkers correspond to gene products from one or more of GABRA3, CTAG2, MAGEA6, SOHLH1, MAGEA1, AFAP1-AS1; CBX2, LINC00484, KIF7, TMSB15A, NEK2, NTRK1, CCND2, NES, PKP2, C1orf226, IFITM1, CDH23, AGRN, DHX58, and LINC02576. A method of diagnosing and treating multiple myeloma in a subject comprises, (a) measuring the level of one or more biomarkers in a sample; (b) comparing the level of the one or more biomarkers to a reference level of the one or more biomarkers; (c) making a diagnosis based on the result of the comparing step; and (d) treating the subject with one or more active agents where the subject is diagnosed with multiple myeloma.
Resumen de: WO2024218320A1
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 checkpoint-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 transmembrane domain.
Nº publicación: EP4698192A2 25/02/2026
Solicitante:
HACKENSACK MERIDIAN HEALTH INC [US]
Hackensack Meridian Health, Inc
Resumen de: US2024360236A1
The present disclosure provides a method for treating an eligible subject with acute myeloid leukemia including high-risk disease features comprising administering to the subject post-consolidation a targeted immunotherapy comprising an immunotherapeutic agent specifically targeting B cell maturation antigen.
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