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52
results.
Updated on
30/04/2025 [06:45:00]
Absstract of: WO2025085525A2
The present disclosure provides methods for treating acute myelogenous leukemia (AML) in a subject in need thereof comprising administering to the subject an effective amount of an anti-PD-L1 antibody or antigen binding fragment thereof and cytokine induced memory-like natural killer (CIMN) cells.
Absstract of: WO2025085792A1
Disclosed herein are combined therapies for treating a hematologic malignancy (e.g., acute myeloid leukemia (AML), or myelodysplastic syndromes (MDS)), using an antibody that binds human galectin-9 (anti-Gal9 antibody, e.g., G9.2-17), and one or more chemotherapeutics, e.g., a Bcl2 inhibitor such as venetoclax, a hypomethylating agent (HMA), or a combination thereof.
Absstract of: WO2025081518A1
Provided is the use of DPP4 as an NK/T cell lymphoma tumor marker, the use of a DPP4 detection reagent in preparing a kit for screening for NK/T cell lymphoma, and the use of a DPP4 inhibitor in preparing a medicine for treating NK/T cell lymphoma.
Absstract of: US2025129435A1
The present disclosure provides a novel method of diagnosing lymphoma, breast cancer, a lymphoma subtype, or a breast cancer subtype in a patient, and kits for implementing the methods.
Absstract of: US2025127751A1
The disclosure belongs to the technical field of medicine, and specifically discloses a traditional Chinese medicine compound preparation for tumors and application thereof. The traditional Chinese medicine compound preparation includes dimethylarsenic acid, indirubin and cordycepin in a concentration ratio of (1-20):(1-10):(1-40). The traditional Chinese medicine compound preparation of the disclosure can be used for treating kinds of tumors, including leukemia, gastric cancer, lung cancer, glioma, papillary thyroid carcinoma, growth hormone adenoma, pituitary adenoma, myeloma, and other malignant tumors. The traditional Chinese medicine compound preparation has significant treatment effect, high safety, and good development prospects.
Absstract of: WO2025085878A1
The present invention relates to compounds of formula (A) as DUX4 inhibitors for the treatment of e.g. neuromuscular disorders, inflammatory disorders, facioscapulohumeral muscular dystrophy, B-cell leukemia, sarcomas, solid cancers, rheumatoid arthritis, axial spondylarthritis, viral infections, mononucleosis, encephalitis, and varicella. Exemplary compounds are e.g.
Absstract of: US2025129162A1
The invention 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 (CD3) bispecific antibodies.
Absstract of: US2025129420A1
There is a need for improved methods for determining the diagnosis and prognosis of patients with conditions, including autoimmune disease and cancer, especially lymphoid neoplasms, such as lymphomas and leukemias. Provided herein are methods for using DNA sequencing to identify personalized, or patient-specific biomarkers in patients with lymphoid neoplasms, autoimmune disease and other conditions. Identified biomarkers can be used to determine and/or monitor the disease state for a subject with an associated lymphoid disorder or autoimmune disease or other condition. In particular, the invention provides a sensitive method for monitoring lymphoid neoplasms that undergo clonal evolutions without the need to development alternative assays for the evolved or mutated clones serving as patient-specific biomarkers.
Absstract of: US2025127855A1
A method of treating chronic myelomonocytic leukemia or myelodysplastic syndrome in a subject in need thereof, comprising the steps of: (a) administering intravenously to the subject for the chronic myelomonocytic leukemia about 2.0 mg/kg body weight per day of a recombinant fusion protein of SEQ ID NO: 1 in the form of a composition comprising a pharmaceutically acceptable excipient and the recombinant fusion protein, (b) about 65 minutes to about 75 minutes after completing the administering of step (a), administering subcutaneously to the subject about 75 mg/m2 of azacitidine, and (c) after steps (a) and (b), repeating step (a) once weekly, and administering subcutaneously to the subject about 75 mg/m2 of azacitidine once daily, wherein on the days that the subject is also having step (a) repeated, the azacitidine is administered about 65 minutes to about 75 minutes after completing the repeated administering of step (a).
Absstract of: US2025127755A1
Disclosed herein are methods for using an antimalarial endoperoxide compound, such as artemisinin, in treating a subject suffering from myelodysplastic syndromes (MDS), and hi slowing or preventing the progression of MDS in the subject to development of acute myeloid leukemia (AML).
Absstract of: US2025129431A1
The invention features methods for the identification of genomic aberrations in circulating tumor cells (CTCs) isolated from peripheral blood. In various embodiments of the disclosure, the methods involve isolation of a small number of purified circulating multiple myeloma cells, purification of genomic DNA from the cells, and sequencing of the genomic DNA.
Absstract of: CN119365214A
Methods of treating diffuse large B-cell lymphoma (DLBCL) or increasing, enhancing, or stimulating an immune response with antibodies and antigen-binding fragments thereof that specifically bind to TIGIT (T cell immune receptors with Ig and ITIM domains) in combination with an anti-PD1 antibody and/or an anti-CD20 antibody are provided.
Absstract of: WO2025080924A1
Provided herein is a recombinant adeno-associated virus (rAAV) comprising an AAV capsid and an expression cassette comprising an engineered nucleic acid sequence encoding an anti-hCD20 antibody (i.e., rituximab) comprising heavy chain and light chain operably linked to regulatory control sequences which direct expression of rituximab in a target cell. Also provided are a pharmaceutical composition comprising a rAAV as described herein in a formulation buffer, nucleic acid molecule, packaging host cells, rAAV production system, and a method of treating CD20-positive central nervous system lymphomas
Absstract of: WO2025080942A1
The present disclosure provides proteasome inhibitors of Formula (I), useful in treating cancer, such as multiple myeloma and mantle cell lymphoma.
Absstract of: WO2025080543A1
Provided herein are methods of predicting the responsiveness of a lymphoma patient to a cancer treatment. Also provided herein are methods of treating a lymphoma patient based on predicting the responsiveness of the lymphoma patient to a cancer treatment.
Absstract of: WO2025080282A1
The present disclosure provides methods for treating leukemia (e.g., AML) using a CLK/DYRK inhibitor and a B-cell lymphoma 2 (BCL2) inhibitor (e.g., venetoclax). Kits for use in practicing the methods are also provided.
Absstract of: US2025122295A1
The invention provides a method for the treatment of Ph+ leukemia in a patient comprising administering to the patient (i) a BCR-ABL tyrosine kinase inhibitor, and (ii) an agent which selectively binds to a cell surface receptor expressed on Ph+ leukemic stem cells. The invention further provides for the use of (i) and (ii) in, or in the manufacture of a medicament for, the treatment of Ph+ leukemia in a patient; and a composition for the treatment of Ph+ leukemia in a patient comprising (i) and (ii); and kits comprising (i) and (ii). In some embodiments, the tyrosine kinase inhibitor is or is not imatinib; or is selected from the group consisting of dasatinib, nilotinib, bosutinib, axitinib, cediranib, crizotinib, damnacanthal, gefitinib, lapatinib, lestaurtinib, neratinib, semaxanib, sunitinib, toceranib, tyrphostins, vandetanib, vatalanib, INNO-406, AP24534, XL228, PHA-739358, MK-0457, SGX393 and DC2036; or is selected from the group consisting of dasatinib and nilotinib. In some embodiments, the agent binds to a receptor involved in signalling by at least one of IL-3, G-CSF and GM-CSF. In some embodiments, the agent is a mutein selected from the group consisting of IL-3 muteins, G-CSF muteins and GM-CSF muteins. In some embodiments, the mutein is an IL-3 mutein. In some embodiments, the agent is a soluble receptor which is capable of binding to IL-3.
Absstract of: US2025122297A1
Disclosed herein is a method of treating cancer, such as multiple myeloma, involving the combination of an anti-BCMA antigen binding protein (e.g., an anti-BCMA antibody) and an immunomodulatory drug (e.g. pomalidomide or lenalidomide). The combinations can also include an anti-inflammatory compound (e.g. dexamethasone).
Absstract of: US2025122300A1
Isolated anti-human CD45RC antibodies or binding fragments thereof, nucleic acids and expression vector encoding the same, compositions including the same, and uses thereof as medicaments, including for the prevention and/or treatment of CD45RChigh-related diseases (including autoimmune diseases, undesired immune responses, monogenic diseases, and lymphoma or cancer), in particular for use in preventing and/or treating graft-versus-host disease (GVHD).
Absstract of: US2025120947A1
The present invention generally relates to sensitizer compounds and their use to sensitize cancer and/or pre-cancerous cells of certain cancers to treatment with certain resistance-prone therapeutics used in cancer therapy. In embodiments, the conjugates of particular esters or amides of Near Infrared Dyes, are used as sensitizers to avoid or overcome therapeutic resistance once formed. In embodiments, the sensitizers include conjugates with Cisplatin, Simvastatin, Artemisinin, platin-based compounds or statins. In embodiments, the resistance prone cancer therapeutics include cisplatin, gemcitabine, doxorubicin, paclitaxel, docetaxel, and platin-based compounds. These may be administered in combination with the sensitizer, or the sensitizer itself may comprise an therapeutci-derived moiety conjugated to the sensitizer, for example as is the case for dye-CIS conjugated sensitizers. Alternatively, the sensitizer may be co-administered with one or more therapeutic. Embodiments of the invention may advantageously be used in cancers that have a tendency to develop resistance to such cancer therapeutics and/or to form metastases, including e.g. lung, pancreatic, prostate, testicular, ovarian, cervical, bladder, breast, head and neck, esophageal, and stomach, cancers, germ cell tumors, lymphomas and other cancers.
Absstract of: US2025123282A1
Disclosed here are methods of evaluating resistance to a tyrosine kinase inhibitor (TKI) therapy of acute myeloid leukemia (AML) in a subject that include detecting the status of CD33, CD44, and phosphorylated BCL2 associated agonist of cell death (pBAD) expression. Also disclosed herein are methods of treating AML in a subject by administering a TKI and one or more inhibitors targeting a TKI-activated compensation pathway to the subject.
Absstract of: AU2022476674A1
The present disclosure relates generally to methods of treating T-cell lymphomas with combination therapies.
Absstract of: US2025121001A1
A method of enhancing embryo implantation in a subject is disclosed which comprises administering to the uterine cavity of the subject a formulation comprising copper and/or zinc in an amount effective to stimulate endometrial production of leukaemia inhibitory factor (LIF) and/or vascular endothelial growth factor (VEGF). Alternatively, a device may be inserted into the uterine cavity of the subject, wherein the device comprises copper and/or zinc, for a period of time that is effective to stimulate endometrial production of LIF and/or VEGF. The method is suitable for use with women undergoing treatment by any of the assisted reproductive technologies, such as those involving the transfer of embryos such as in vitro fertilisation (IVF) and variants including IVF-ICSI (intracytoplasmic sperm injection) and in vitro maturation (IVM) treatments, as well as intrauterine-insemination (IUI) therapy. However, the method is also applicable for women wanting to improve their prospects of pregnancy through natural conception.
Absstract of: WO2025080753A1
The present invention relates to bifunctional compounds, which find utility to degrade and (inhibit) one or more of the following kinases: DYRK1A, DYRK1B, DYRK2, DYRK3, DYRK4, CLK1, CLK2, CLK3, CLK4, CDK7, CDK8/19, PI3K, PDGFrA/B, mTOR, HIPKs, and/or CMGC kinases leading to inhibition of WNT signaling. In particular, the present invention is directed to compounds, which contain on one end an E3 ubiquitin ligase binding moiety which binds to an E3 ubiquitin ligase and on the other end a moiety which binds one or more of the following kinases: DYRK1A, DYRK1B, DYRK2, DYRK3, DYRK4, CLK1, CLK2, CLK3, CLK4, CDK7, CDK8/19, PI3K, PDGFrA/B, mTOR, HIPKs, and/or CMGC kinases leading to inhibition of WNT signaling, such that the one or more kinases is placed in proximity to the ubiquitin ligase to effect degradation (and inhibition) of the one or more kinases. The bifunctional compounds serve as therapeutics for the treatment of Alzheimer's disease, down syndrome, diabetes, an autoimmune disease, an inflammatory disorder (e.g., airway inflammation, osteoarthritis (e.g., knee related osteoarthritis)), cancer (e.g., glioblastoma, prostate cancer, metastatic breast cancer, metastatic lung cancer, multiple myeloma, secondary metastatic tumors of the brain, colorectal cancer, acute myeloid leukemia, myelodysplastic syndrome), a viral infection (e.g., SARS-CoV-2 infection (e.g., COVID-19)), and other diseases.
Nº publicación: WO2025078334A1 17/04/2025
Applicant:
INSTITUT NATIONAL DE LA SANTE ET DE LA RECH MEDICALE [FR]
ASSIST PUBLIQUE HOPITAUX DE PARIS APHP [FR]
CENTRE NATIONAL DE LA RECHERCHE SCIENT [FR]
UNIV PARIS CITE [FR]
PUISSANT ALEXANDRE [FR]
INSTITUT NATIONAL DE LA SANT\u00C9 ET DE LA RECHERCHE M\u00C9DICALE,
ASSISTANCE PUBLIQUE-H\u00D4PITAUX DE PARIS (APHP),
CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE,
UNIVERSIT\u00C9 PARIS CIT\u00C9,
PUISSANT, Alexandre
Absstract of: WO2025078334A1
Chemotherapy resistance is the major therapeutic barrier in acute myeloid leukemia (AML). To address this issue, the inventors generated a syngeneic mouse model of AML, which we evolved to develop resistance to a front-line chemotherapy regimen. The inventors identified SRRM1 as a critical vulnerability of chemoresistant leukemic cells and identified that PAK1 and CLK kinases are regulators of SRRM1 in chemoresistant AML cells. Human and murine chemoresistant cells were found to be markedly more sensitive to inhibitors of PAKs (FRAX597) and CLKs (TG003 and ML 167) compared to their naive counterparts, an effect which was even further enhanced by treatment with cytarabine and daunorubicin. Simultaneous suppression of Clk1 and Pak1 or Clk-4 and Pak1 using validated shRNAs and combinations of FRAX597 and TG003, or FRAX597 and ML 167 synergized to reduce the growth and the colony-forming capacity of chemoresistant AML cells and sensitized them to chemotherapy. The combined treatment improved overall mouse survival and reduced disease burden in the chemoresistant AML mouse models. Moreover, AML patient cells that were primarily refractory or from a post chemotherapy relapse (n=21 ) exhibited a higher ex vivo sensitivity to the FRAX597 + TG003 combination in comparison with chemosensitive patients at diagnosis (n=28). Finally, combined PAK1 and CLK inhibition more effectively reduced disease progression in animals transplanted with the relapse sample than in those engrafted with th
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