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61
resultados
Última actualización
25/11/2025 [06:45:00]
Resumen de: US2025353854A1
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.
Resumen de: WO2025237908A1
The present invention relates to the field of the treatment of cancer. In this study, the inventors found that VDAC2 is heterogeneously expressed in MM cells. VDAC2 protein expression correlated with BAK but not with BAX protein levels. Transient silencing of VDAC2, but not VDAC1 or VDAC3, sensitized MM cells to intrinsic mitochondrial apoptosis signals, alongside with the induction of pre-activated BAK and the increase of global, MCL1 and BCL2 mitochondrial priming. They also found a that a VDAC2 compound, efesevin recapitulated the sensitization effect of VDAC2 knock-down on BH3 mimetics apoptotic response. This novel VDAC2 modulator sensitized MM cells to BH3 mimetics targeting MCL1 (S63845) or BCL2 (Venetoclax) without modifying BAK or BAX protein expression. The efficiency of the VDAC2 modulator was directly correlated with the levels of VDAC2 protein. To better understand the VDAC2/BAK interplay, The inventors generated VDAC2 KO myeloma cells. VDAC2 KO cells exhibited an important decrease of BAK protein expression while BAX remained unchanged. Accordingly, VDAC2 KO cells completely lost their mitochondrial priming. Interestingly, they also found that BAK KO myeloma cells displayed decreased levels of VDAC2. The reciprocal regulation between VDAC2 and BAK was dependent on both the proteasome and lysosome degradation pathways. Thus, the present invention relates to a combination of a VDAC2 modulator and a BH3- mimetics compound for use in the treatment of a cancer in a s
Resumen de: US2025352582A1
The present invention includes compositions and methods for treating AML utilizing bispecific CARs. In certain aspects, the invention includes a bispecific split CAR which binds CD13 and TIM-3 on AML cells.
Resumen de: AU2025259861A1
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. Arsenic treatment has shown great promise in the treatment of several cancers but requires daily intravenous (IV) administration. This invention relates to a novel formulation comprising a lyophilized compositions comprising arsenic. As a result, the formulation facilitates a systemic bioavailability comparable to that of intravenous (IV) administration of arsenic trioxide currently practiced. 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. 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
Resumen de: AU2024261833A1
Provided herein are methods comprising multifunctional binding proteins comprising a first and a second antigen binding domain and all or part of an immunoglobulin Fc region or variant thereof, wherein the first antigen binding domain binds specifically to CD123 and the second antigen binding domain binds specifically to human NKp46, and wherein all or part of the immunoglobulin Fc region or variant thereof bind to a human Fc-γ receptor, for the treatment or prevention of leukemias and myelodysplastic disorders.
Resumen de: WO2025236094A1
Identification, Design and Validation of Public Neoantigens and Tumor-associated Antigen vaccines for the Prevention and Treatment of Down Syndrome-associated Leukemia.
Resumen de: WO2025240852A1
In one aspect, the disclosure relates to composition and methods for proteolysis-targeting chimeric molecules (PROTACs). In some aspects, the disclosed compounds are useful for modulating LCK tyrosine kinase activity through targeted degradation. In some aspects, the disclosed compounds are orally bioavailable. In further aspects, the present disclosure relates to methods of making the disclosed compounds, pharmaceutical compositions comprising the disclosed compounds, and methods of treating various clinical conditions and disorders using the same, such as T-cell acute lymphoblastic leukemia. 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 disclosure.
Resumen de: US2025354218A1
The present technology relates to methods for predicting the risk of acute myeloid leukemia (AML) in a subject prior to the onset of AML symptoms, and whether such a subject will benefit from treatment with an AML therapy. The methods disclosed herein are based on detecting the presence of mutations in the nucleic acid sequences of IDH1/2, TP53, DNMT3A, TET2, and spliceosome genes. Kits for use in practicing the methods are also provided.
Resumen de: AU2024243824A1
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: AU2025259981A1
The invention relates to combination therapies, particularly combination therapies for the treatment of myeloid malignancy. The combination therapies are particularly useful in methods for the treatment of acute myeloid leukemia (AML). The combination therapies 5 include an antibody or antigen binding fragment thereof that binds to CD70 and a BCL-2 inhibitor, preferably venetoclax or a pharmaceutically acceptable salt thereof. 10 15 20 25 The invention relates to combination therapies, particularly combination therapies for the treatment of myeloid malignancy. The combination therapies are particularly useful in 5 methods for the treatment of acute myeloid leukemia (AML). The combination therapies include an antibody or antigen binding fragment thereof that binds to CD70 and a BCL-2 inhibitor, preferably venetoclax or a pharmaceutically acceptable salt thereof. ct c t
Resumen de: WO2025233264A1
The present invention relates to antibodies that inhibit the enzymatic activity of human CD73, for use in enhancing the activity of T-cell engager therapies in the treatment of disease, notably B-cell Non-Hodgkin Lymphoma.
Resumen de: WO2025233266A1
The present invention relates to agents that inhibit the enzymatic activity of human CD39, for use in enhancing the activity of T-cell engager therapies in the treatment of disease, notably B cell Non-Hodgkin Lymphoma.
Resumen de: US2025346890A1
The present invention relates to an inhibitor of R-spondin 2 and/or R-spondin 3 mediated bone morphogenetic protein (BMP) receptor inhibition for use in treating and/or preventing leukemia in a subject; and to methods, kits, combined preparations, and uses related thereto.
Resumen de: WO2025235642A1
Methods for treating and/or assessing a subject having a symptomatic multiple myeloma or a precursor thereof, where the methods involve characterizing a plasma cell dyscrasia (e.g., monoclonal gammopathy of undetermined significance, smoldering multiple myeloma, multiple myeloma, plasma cell leukemia) in a biological sample from a subject as being high, medium, or low risk by assigning to the plasma cell dyscrasia a multiple myeloma (MM)-like score. The methods may involve sequencing DNA from the biological sample using whole-genome sequencing (WGS).
Resumen de: WO2025235924A2
Methods and uses of immunoconjugates that bind to CD123 (e.g., pivekimab sunirine) in patients with acute myeloid leukemia (AML) are provided. Such immunoconjugates can be used as monotherapies or can be used in combination with BCL-2 inhibitors (e.g., venetoclax), and/or hypomethylating agents (e.g., azacitidine or decitabine) to prepare patients with AML for hematopoietic stem cell transplant and/or to achieve complete remissions in patients with AML, including those with poor prognostic markers.
Resumen de: US2025346582A1
In accordance with the purpose(s) of the present disclosure, as embodied and broadly described herein, the disclosure, in one aspect, relates to compounds (I) that are inhibitors for spleen tyrosine kinase (Syk), which is a key signaling protein in hematologic cells and implicated in multiple hematopoietic malignancies, cancer (e.g., chronic lymphoid leukemia (CLL) or acute myeloid leukemia (AML)), diabetes, and immune disorders. In one aspect, the compounds described herein drug resistance, which renders current ATP-competitive Syk inhibitors ineffective.
Resumen de: US2025347699A1
This disclosure relates to a method of expressing the receptor-binding domain (RBD) region of the coronavirus SARS-CoV-2 Spike protein in a highly native form that is strongly reactive to natural antibodies induced upon SARS-CoV-2 infection or vaccination of humans and that more efficiently binds the angiotensin-converting enzyme 2 (ACE2) receptor. This method fuses the RBD to the C-terminus of an N-terminal fragment of the gp70 protein (the surface protein (SU) of the Friend57 strain of murine leukemia viruses). This method of expression enhances the native folding of the RBD and increases its recognition by antibodies present in immune sera and its ability to interact with the ACE2 receptor. Further disclosed are methods of using this form of RBD for various purposes.
Resumen de: MX2025007460A
Methods of monitoring therapeutic efficacy in a subject with myelodysplastic syndrome (MDS) are provided. Also provided is a method of identifying a subject with MDS for treatment with a telomerase inhibitor, and methods of treating MDS. The methods include administering to the subject a telomerase inhibitor and assessing variant allele frequency (VAF) for one or more of the following genes: SF3B1, TET2, DNMT3A, ASXL1, and CUX1 in a biological sample obtained from the subject after administration of the telomerase inhibitor. In some cases, a 25% or more reduction in VAF identifies a subject who has an increased likelihood of benefiting from treatment with a telomerase inhibitor. In some instances, the telomerase inhibitor is imetelstat or imetelstat sodium.
Resumen de: US2025339429A1
The present disclosure provides methods for treating ULK3-associated cancers, such as multiple myeloma or breast cancer, in subjects in need thereof.
Resumen de: WO2025231449A1
The present disclosure provides improved compositions and methods for detecting, diagnosing, prognosing, monitoring, and treating hematological disorders including multiple myeloma in a subject. In particular, the disclosure provides methods for detecting IL4I1 in subjects to reliably diagnose, predict survival, or monitor multiple myeloma in the subject and methods for inhibiting IL4I1 to treat multiple myeloma in the subject.
Resumen de: WO2025231299A1
The present disclosure relates to HA-1-targeted T cell receptor (TCR) T cell therapy for treating hematological cancer, such as recurrent leukemia after hematopoietic stem cell transplantation. Provided embodiments include T cell compositions and methods of using the same in therapy, as well as methods of making the compositions. Provided embodiments further include CD8+ T cells made by a method and methods for making CD8+ T cells.
Resumen de: AU2024264188A1
The present disclosure provides crystalline free base and salts of an imidazo1,2- bpyridazine compound. In some embodiments, the crystalline imidazo1,2-bpyridazine compound is a single crystal. The present disclosure also provides methods of using the crystal forms to treat certain diseases or disorders. Some embodiments include methods of using the crystal forms to treat hematopoietic cancers, myelodysplastic syndromes (MDS), or acute myeloid leukemia (AML). Additional embodiments provide disease treatment using the crystal forms in combination with other therapies, such as cancer therapies.
Resumen de: AU2024239549A1
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.
Nº publicación: US2025339406A1 06/11/2025
Solicitante:
THE REGENTS OF THE UNIV OF MICHIGAN [US]
The Regents of the University of Michigan
Resumen de: US2025339406A1
Provided herein are small molecule inhibitors of NSD1, NSD2 and/or NSD3 activity, and methods of use thereof for the treatment of disease, including leukemia, breast cancer, osteosarcoma, lung and prostate cancers and other solid tumors as well as other diseases dependent on the activity of NSD1, NSD2 and/or NSD3.
BOPI
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