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95
results.
Updated on
07/06/2025 [07:56:00]
Results 75 to 95 of 95
Absstract of: WO2025096757A1
The present disclosure provides methods of treating a subject having or suspected of having a B cell malignancy or a B cell mediated disorder by administering hypoimmune allogenic CD22-directed CAR T cells. Also disclosed are pharmaceutical compositions comprising hypoimmune allogenic CD22-directed CAR T cells, for use in treating a subject having or suspected of having a B cell malignancy or a B cell mediated disorder.
Absstract of: WO2025096717A1
Embodiments of the present invention relate to methods of treating multiple myeloma in a subject in need thereof comprising administering to the subject a BCMAxCD3 bispecific antibody on a monthly dosing schedule.
Absstract of: WO2025093886A1
The present invention relates to anti-CD24 antibodies for use in the treatment of myelofibrosis, thrombosis, essential thrombocythemia (ET) and/or juvenile myelomonocytic leukaemia (JMML).
Absstract of: WO2025094085A1
Embodiments of the present invention relate to methods of treating multiple myeloma in a subject in need thereof by administering therapeutically effective combination regimens comprising a GPRC5DxCD3 bispecific antibody and one or more of pomalidomide, daratumumab or lenalidomide.
Absstract of: WO2025093666A1
The invention relates to the field of medicine, more specifically to treatment of lymphoma.
Absstract of: US2025144100A1
The present invention relates to a tablet composition comprising Ibrutinib and one ore more pharmaceutically acceptable excipients. The invention further relates to the use of said composition as a medicament, particularly in the treatment of lymphocytic leukaemia (CLL), mantle cell lymphoma (MCL), Waldenström's macroglobulinaemia (WM) and chronic graft versus host disease (cGVHD).
Absstract of: US2025144189A1
The present disclosure provides a novel recombinant unidirectional asparagine racemase for the conversion of L-asparagine to D-asparagine. Such unidirectional asparagine racemase could be used in treating cancers (e.g., leukemias or lymphomas) that require exogenous L-asparagine. This innovative design offers a promising new approach to reduce detrimental side effects caused by current therapies.
Absstract of: US2025145635A1
A compound containing a bis(azanylylidene) sulfonyl structure of formula (I) as a PKR agonist and/or USP9X inhibitor, which can be used for treating related diseases mediated and regulated by PKR and USP9X, wherein the related diseases comprise, but are not limited to: sickle-cell anemia, β-thalassemia, hereditary non-spherocytic hemolytic anemia, hemolytic anemia, hereditary spherocytosis, hereditary elliptocytosis, abetalipoproteinemia, paroxysmal nocturnal hemoglobinuria, acquired hemolytic anemia, congenital anemia, anemia of chronic diseases, colorectal cancer, kidney cancer, pancreatic cancer, breast cancer, lung cancer, esophageal cancer, melanoma, lymphoma, glioblastoma, or multiple myeloma.
Absstract of: US2025145706A1
The present invention provides antibodies for the treatment of chronic lymphocytic leukemia (CLL). These antibodies target the B-cell receptor (BCR) of CLL cells characterised by R110-mutated immunoglobulin lambda variable 3-21 (IGLV3-21R110). The invention also provides nucleic acid sequences encoding the forgoing antibodies, vectors containing the same, pharmaceutical compositions and kits with instructions for use.
Absstract of: WO2025096203A1
Chimeric RNAs and their protein products, including BCR-ABL in chronic myelogenous leukemia and EML4-ALK4 in lung cancer, have been well-established as ideal biomarkers and drug targets for malignant cancers. Using RNA-Sequencing data from The Cancer Genome Atlas (TCGA) database, a chimeric RNA SLC2A11-MIF was identified that is present in nearly 50% of CRC samples but absent in non-cancer colon tissue. Disclosed herein is a method for diagnosing and treating cancers expressing this chimeric RNA and protein.
Absstract of: WO2025096605A1
The present disclosure relates to methods of treating a subject having multiple myeloma, including refractory/resistant multiple myeloma, comprising administering to the subject a CD73 inhibitor and an anti-CD38 agent.
Absstract of: WO2025097015A1
Targeted therapeutics for the treatment of cancers that express CLEC2A are described. The targeted therapeutics include anti-CLEC2A binding domains and engineered formats thereof such as multi-domain binding molecules, antibody conjugates, and recombinant receptors expressed by an immune cell. The targeted therapeutics can be used to treat acute myeloid leukemia (AML), such as KMT2A-r AML cell. Furthermore, the binding domains can be used to isolate cells expressing CLEC2A or to target such cells ex vivo or in vivo for research, diagnostic, or therapeutic purposes.
Absstract of: WO2025096532A1
Provided herein are methods for monitoring, identifying, assessing, circulating tumor DNA (ctDNA) for treating a subject or monitoring a subject having cancer, and related methods and uses thereof. In some embodiments, the disease or condition is a B cell lymphoma (BCL) relapsed or refractory.
Absstract of: WO2025097150A1
Provided herein are methods of preparing an immunotherapeutic with enhanced efficacy by treating lymphocytes with a B-cell lymphoma 2 (BCL-2) inhibitor, immunotherapeutic compositions produced by the methods herein, and methods of treating cancer therewith.
Absstract of: WO2025097146A1
Provided are methods for treating an individual diagnosed with multiple myeloma (MM) by administering to the individual a therapeutically effective amount of a C-X-C motif chemokine receptor 2 (CXCR2) inhibitor to thereby inhibit progression of the MM. Combining CXCR2 blockade with standard of care agents has a synergistic anti-MM effect. Also provided are characterizations of MM patient neutrophils with identification of markers that reveal distinct subsets of neutrophils found in bone marrow and focal lesions of MM patients.
Absstract of: WO2025097084A1
Familial Platelet Disorder (FPD) is associated with germline RUNX1 mutations, establishing a preleukemic state and increasing the risk of developing acute leukemia. Conventional approaches lack intervention strategies that may delay or prevent leukemia progression in patients. The present disclosure integrates single-cell transcriptomics, flow cytometry, and spatial proteomics data analyses for a large cohort of FPD patient samples to show that RUNX1 mutations unleash inflammatory signaling in familial platelet disorder. Specifically, the receptor CD74 has been identified as a biomarker and a master regulator of downstream signaling pathways. Embodiments of the present disclosure provide diagnostic and treatment methods for FPD in patients.
Absstract of: WO2025092884A1
Provided is a method for treating chronic-phase and/or accelerated-phase and/or blast-phase chronic myelogenous leukemia and/or acute lymphoblastic leukemia in a subject by administering to the subject a compound of formula (I) or a pharmaceutically acceptable salt, crystal form, solvate or hydrate thereof. Also provided is a use of the compound of formula (I) or the pharmaceutically acceptable salt, crystal form, solvate or hydrate thereof in combination with an ATP-competitive BCR-ABL1 inhibitor.
Absstract of: AU2025202743A1
The present disclosure provides compositions and methods for targeting a minor histocompatibility (H) antigen (HA-1H) to, for example, prevent or manage relapse of a hematological malignancy after allogeneic hematopoietic stem cell transplantation (HCT). Also provided are transgene constructs encoding engineered binding proteins, such as a T cell receptor or a chimeric antigen receptor, optionally encoding additional components such as a co-receptor and/or safety switch. Such transgene constructs can be transduced into an immune cell, such as a T cell, and used as an immunotherapy in a subject having a hematological malignancy or at risk for recurrence of the hematological malignancy (e.g., leukemia, lymphoma, myeloma).
Absstract of: AU2023362608A1
The present invention relates to means and methods to prevent and/or treat Epstein-Barr virus (EBV) and EBV-induced diseases, such as EBV infection, infectious mononucleosis (IM), malignant or non-malignant post-transplant lymphoproliferative disorder (PTLD) and other EBV-associated diseases. In particular, the invention provides a SQAPLPCVL peptide that can be used in a treatment or a method of treatment to induce an EBV-specific immune response in a subject. The SQAPLPCVL can be used in a treatment or method of treatment as a vaccine against EBV and EBV-induced diseases. It is preferred herein that Epstein-Barr virus (EBV) and/or EBV-induced diseases are prevented.
Nº publicación: WO2025096692A2 08/05/2025
Applicant:
TARAN THERAPEUTICS INC [US]
THE UNIV OF ADELAIDE [AU]
TARAN THERAPEUTICS, INC,
THE UNIVERSITY OF ADELAIDE
Absstract of: WO2025096692A2
Provided herein are methods for treating a subject having chronic myelomonocytic leukemia (CMML), the method comprising: (a) identifying a RAS pathway mutation in tumor cells of the subject, wherein the RAS pathway mutation is a NRAS, KRAS, PTPN-11 and/or CBL mutation; (b) identifying a dominant CBL mutation of CBL variant allele frequency of from <5% to >10%; and (c) administering to the subject identified in step (a) a therapeutically effective amount of an anti-hGM-CSF antibody. Also provided herein are methods for treating a subject having chronic myelomonocytic leukemia (CMML), the method comprising: (a) identifying a RAS pathway mutation in tumor cells of the subject, wherein the RAS pathway mutation is a NRAS, KRAS, PTPN-11 and/or CBL mutation; (b) identifying a dominant CBL mutation of CBL variant allele frequency of from <5% to >10%; and (c) administering to the subject identified in step (a) a therapeutically effective amount of an anti-hGM-CSF antibody lenzilumab and a therapeutically effective amount of a second therapeutic agent. The subject may have a RAS pathway mutation or a RAS pathway mutation and at least one TET2 mutation identified in the tumor cells, an increased percentage of CD116 and CD131 in CD34+ stem and progenitor cells in the subject compared to a healthy subject and/or an increased percentage of CD14+ cells in the subject compared to a healthy subject. A therapeutically effective amount of a hypomethylating agent or hydroxyurea may b
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