Resumen de: US20260069584A1
The present invention relates to methods of treating leukemia using Tyrosine Kinase inhibitors. The invention particularly relates to methods of treating CML and ALL using a compound of Formula I or a pharmaceutically acceptable salt thereof. The compound of Formula 1 has been shown to be efficacious safe and tolerable at a dose from 10 mg to 210 mg.
Resumen de: AU2024317966A1
The present disclosure provides antigen-binding proteins specifically binding GPRC5D, as well as respective antibodies in enhanced ADCC formats, and methods of using them to treat cancers such as multiple myeloma.
Resumen de: WO2026055296A2
Methods of producing Minute Mouse Virus (MMV) stock are described herein. Methods of producing xenotropic murine leukemia virus (xMuLV) stock are described herein.
Resumen de: WO2026055403A1
Provided are compounds of the Formula PTM-L-CLM, or a pharmaceutically acceptable salt thereof, wherein the PTM is (PTM-I) These compounds are useful for the degradation of BCL6 and in the treatment cancer.
Resumen de: US20260069567A1
The disclosure herein provides combination therapies for the treatment of cancers such as Leukemia, lymphoma and triple negative breast cancer. The disclosure provides combination therapies of CDK inhibitors, e.g., a CDK inhibitor represented by Formula I:or a pharmaceutically acceptable salt thereof together with a BCL-2 inhibitor or proteasome inhibitor for the treatment of cancer.
Resumen de: US20260069625A1
The present disclosure relates to RNAi agents useful in methods of treating KRAS-related diseases such as a proliferative disease, including without limitation a solid or liquid cancer, adenocarcinoma, colorectal cancer, advanced and/or metastatic colorectal cancer, colon cancer, lung, non-small cell lung cancer and lung adenocarcinoma, acute myelogenous lung, bladder, brain, breast, cervical, endometrial, gastric, head and neck, kidney, leukemia, myelodysplastic syndrome, myeloid leukemia, liver, melanoma, ovarian, pancreatic, prostate, testicular, thyroid cancers, and cardio-facio-cutaneous (CFC) syndrome and Noonan syndrome, and similar and related diseases, using a therapeutically effective amount of a RNAi agent to KRAS.
Resumen de: WO2026055492A1
Disclosed herein are methods of administering a Casitas B-lineage lymphoma proto-oncogene B inhibitor (CBL-Bi) for treating a cancer in a subject. Additionally disclosed herein are methods of administering a pre-treatment in combination with the CBL-Bi for treating a cancer in a subject.
Resumen de: WO2026055333A1
The invention provides methods for treating and selecting cancer patients for therapy using a compound that modulates mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) activity, such as inhibiting MALT1 scaffolding activity.
Resumen de: WO2026054717A1
Disclosed herein are methods of enhancing the abundance of NKG2C+ adaptive NK cells in a population of NK cells and the use of NK cells expressing NKG2C derived from such methods for treatment of cancers, including leukemia such as chronic myeloid leukemia with enhanced expression of HLA-E molecule. In one embodiment, the method is a biphasic method comprising a selection phase and an expansion phase. In one embodiment, the selection phase comprises use of a first culture comprising IL-2 and feeder cells expressing HLA-E. In one embodiment, the expansion phase comprises use of a second culture comprising IL-2, IL-15 and feeder cells expressing HLA-E, IL-21 and 4-1 BBL. Also disclosed are methods of stratifying chronic myeloid leukemia patients into responders or non-responders to tyrosine kinase inhibitor to allow a suitable treatment for each group with tyrosine kinase inhibitor or NK cells expressing NKG2C derived from the described methods. In one embodiment, the stratification method comprises determining a percentage of NKG2A+ cells in the patients' NK cell population.
Resumen de: US20260071196A1
The disclosure provides Moloney murine leukemia virus (MMLV) reverse transcriptase (RTase) mutants. The disclosure as provides suitable amino acid positions in MMLV RTase for mutagenesis and methods and kits for using MMLV RTase mutants to synthesize cDNA from RNA templates.
Resumen de: US20260070935A1
Described herein, in part, are bisphosphonate lipid compounds, lipid nanoparticles (LNPs) thereof, and methods of use thereof. In various embodiments, the LNP selectively targets a cell of interest (e.g., a bone cell and/or bone marrow cell, such as a stem cell, stroma cell, osteoblast, osteocyte, osteoclast, bone lining cell, local mesenchymal cell, progenitor cell, mononuclear blood-borne precursor cell, B cell, endothelial cell, granulocytes, T cell, monocytic lineage, B cell lineage, monocytes, cancer cell, tumor cell, tumor cell that metastasize to bone, blood cancer cell, and multiple myeloma cell, inter alia). In other aspects, the present disclosure relates to methods for in vivo delivery of therapeutic agents to prevent or treat diseases, disorders, or conditions using the LNP compositions of the disclosure.
Resumen de: US20260070946A1
The present disclosure, relates, in general to analogs of proline-rich polypeptide 1 (PRP-1) designated tyrosine peptides (TYR peptide) that are useful to treat cancer, such as sarcomas, carcinomas and leukemias or liquid cancers.
Resumen de: US20260070998A1
The present disclosure provides methods for treating multiple myeloma. In certain embodiments, the present methods comprise administering to a subject in need thereof a BCMA inhibitor (e.g., a bispecific antibody or antigen-binding fragment thereof that bind to BCMA and CD3) in combination with a CD38 inhibitor (e.g., an anti-CD38 antibody). In certain embodiments, the subject has been previously treated with one or more anti-cancer therapies.
Resumen de: WO2026055154A1
The present disclosure provides methods and kits for obtaining sequence information of one or more genes from a subject diagnosed with a disease or disorder. Based on the sequence information, the present disclosure further provides methods of predicting a treatment outcome of the subject.
Resumen de: EP4706682A2
A pharmaceutical composition, comprising the compound NSC350625, or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier, for use in a method of treating CNS cancer, lung cancer or lymphoma in a subject.
Resumen de: EP4706673A2
The present disclosure is directed to a combination therapy comprising an anti-CD19 antibody or antibody fragment thereof and gamma delta T-cells (γδ T-cells) for use in the treatment of leukemia or lymphoma.
Resumen de: US20260049279A1
The invention features polypeptides and/or transgenic effector cells including T cell receptors (TCRs) which specifically bind anaplastic lymphoma kinase (ALK) antigens or peptide sequences, and the use of such polypeptides and/or transgenic effector cells and TCRs specific to anaplastic lymphoma kinase (ALK) antigens or peptide sequences in compositions and methods for treating ALK-positive neoplasias such as Non-Small Cell Lung Cancers (NSCLCs).
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: 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: 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: 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: 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: 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: 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.
Nº publicación: WO2026050255A2 05/03/2026
Solicitante:
REGENERON PHARMACEUTICALS INC [US]
REGENERON PHARMACEUTICALS, INC
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.