Resumen de: EP4643952A2
Disclosed are methods for inhibiting proliferation of or inducing apoptosis in certain leukemia cells or both. The methods comprise contacting a leukemia cell exhibiting an NPM1 mutation with a pharmacologic inhibitor of interaction between MLL and menin. More broadly, disclosed are methods for treating a susceptible leukemia using pharmacologic inhibition of Menin-MLL interaction. Also disclosed are methods for treating such leukemias using inhibition of Menin-MLL interaction in combination with DOT1L inhibition.
Resumen de: MX2025009619A
The present invention provides therapeutics for the treatment of CCR9-positive cancers such as T-cell acute lymphoblastic leukemia. In particular, the present invention provides a CCR9 targeting moiety. The present invention furthermore relates to a CCR9 targeting moiety comprising a further targeting moiety, preferably a CD1a targeting moiety, a dual CAR comprising a CCR9 and a CD1a targeting moiety, their use in the treatment of CCR9 and/or CD1a positive cancers, and the use of a CCR9 targeting moiety and a separate CD1a targeting moiety for such treatment.
Resumen de: MX2025008887A
Some embodiments of the invention include inventive compounds (e.g., compounds of Formula (I), (II), or (III)) and compositions (e.g., pharmaceutical compositions) which inhibit IRAK and/or FLT3 and which can be used for treating, for example, certain diseases. Some embodiments include methods of using the inventive compound (e.g., in compositions or in pharmaceutical compositions) for administering and treating (e.g., diseases such as hematopoietic cancers, myelodysplastic syndromes (MDS), acute myeloid leukemia (AML), etc.). Additional embodiments provide disease treatment using combinations of the inventive IRAK and/or FLT3 inhibiting compounds with other therapies, such as cancer therapies.
Resumen de: MX2025011928A
The invention comprises a new and inventive method for conjugating the L-asparaginase enzyme with polyethylene glycol molecules, preferably polyethylene glycol maleimide (PEG-Mal), via cysteine residues present on the surface of the molecule. In addition, the invention relates to the product obtained from this method and the use of the PEG-conjugated enzyme in the treatment of different types of neoplasia, such as acute lymphoid leukaemia.
Resumen de: MX2025012028A
The present invention provides dosing regimens of bispecific antibodies targeting both CD3 and CD20 when used in the treatment of lymphoma, such as B-cell Non-Hodgkin lymphoma (B-NHL).
Resumen de: MX2025012388A
The present invention relates to combinations comprising a therapeutically effective amount of a menin-mixed-lineage leukemia 1 (menin-MLL) inhibitor; and a therapeutically effective amount of a DNA intercalating agent and a pyrimidine analog; as well as to methods for treating a subject diagnosed with cancer using such combinations.
Resumen de: MX2025012452A
The present disclosure provides methods and pharmaceutical compositions for treating or slowing the progression of cancers that overexpress the histone methyltransferase WHSC1, e.g., t(4;14) multiple myeloma, by administering to a subject in need thereof a therapeutically effective amount of an inhibitor of the histone methyltransferase, SETD2.
Resumen de: NZ751414A
The present disclosure describes a pharmaceutical combination of an anti-CD19 antibody MOR00208 and a BCL-2 inhibitor venetoclax for the treatment of non-Hodgkin’s lymphoma, chronic lymphocytic leukemia and/or acute lymphoblastic leukemia.
Resumen de: US2025332216A1
A method of treating classic Hodgkin's lymphoma (cHL) in a subject in need thereof, comprising intravenously administering to the subject i) a recombinant fusion protein at the dose of about 2.0 mg/kg body weight, once a week, and ii) an anti-PD-1 antibody at the dose of about 200 mg, once every 3 weeks, wherein the recombinant fusion protein comprises a mutated SIRPα D1 domain and a functional IgG1 heavy chain constant region, wherein the mutated SIRPα D1 domain comprises the amino acid sequence of SEQ ID NO: 2.
Resumen de: WO2025227007A1
Disclosed herein are 4,6-substituted-2-(3'-1,1'-biphenyl-4-yl)quinoline analogs and pharmaceutically acceptable salts thereof that are inhibitors of dihydroorotate dehydrogenase (DHODH) with properties, including stability and bioavailability as disclosed herein. Also disclosed herein are methods of making the analogs and salts thereof. The disclosed analogs and salts thereof can be used in the treatment of a variety of disorders and diseases in which inhibition of DHODH can be clinically useful, including cancer, such as a hematological cancer, including acute myeloid leukemia (AML); graft-versus-host-diseases; autoimmune disorders; and disorders associated with T-cell proliferation.
Resumen de: WO2025226846A1
Disclosed are substituted purine derivatives of formulae (I), and pharmaceutically acceptable salts, solvates, hydrates, polymorphs, co-crystals, tautomers, stereoisomers, isotopically labeled derivatives, prodrugs, and compositions thereof. Also provided are methods involving the inventive compounds or compositions for treating and/or preventing cell proliferative diseases including certain cancers of breast, brain, ovarian, lung, colorectal cancer, leukemias, lymphoma, melanoma, multiple myeloma, Ewing's sarcoma, osteosarcoma and inflammatory and myotonic dystrophy type 1 diseases in a mammal. Treatment of a subject with a proliferative disease using a compound or composition of the invention may inhibit the aberrant activity of kinases, such as a cyclin-dependent kinases (CDK) (e.g., CDK12/13), and degrade some other proteins (including cycK) and therefore, induce potent antiproliferative and apoptotic effects and/or inhibit transcription in the subject.
Resumen de: WO2025226831A1
Disclosed are purine derivatives of formulae (I), and pharmaceutically acceptable salts, solvates, hydrates, polymorphs, co-crystals, tautomers, stereoisomers, isotopically labeled derivatives, prodrugs, and compositions thereof. Also provided are methods involving the inventive compounds or compositions for treating and/or preventing cell proliferative diseases including certain cancers of breast, brain, ovarian, lung, colorectal cancer, leukemias, lymphoma, melanoma, multiple myeloma, Ewing's sarcoma, osteosarcoma and inflammatory and myotonic dystrophy type 1 diseases in a mammal. Treatment of a subject with a proliferative disease using a compound or composition of the invention may inhibit the aberrant activity of kinases, such as a cyclin-dependent kinases (CDK) (e.g., CDK12/13), and therefore, induce potent antiproliferative and apoptotic effects and/or inhibit transcription in the subject.
Resumen de: WO2025223394A1
The present application relates to a pharmaceutical composition comprising i) a recombinant fusion protein and ii) an anti-PD-1 antibody, wherein the recombinant fusion protein comprises a mutated SIRPα D1 domain linked to a functional IgG1 heavy chain constant region, wherein the mutated SIRPα D1 domain comprises the amino acid sequence of SEQ ID NO: 2. The present application also relates to use of the pharmaceutical composition in preparation of a medicament for treating classic Hodgkin's lymphoma (cHL), e.g., relapsed or refractory cHL.
Resumen de: US2025333445A1
The invention provides a CD16a-binding polypeptide which comprises at least one motif that binds to CD16a, wherein said polypeptide comprises the following structure: N-terminal portion-Helix 1-Separating portion-Helix 2-C-terminal portion the CD16a-binding motif being the portion Helix 1-Separating portion-Helix 2. The invention further provides pharmaceutical compositions comprising the CD16a-binding polypeptide, and the use of the CD16a-binding polypeptide or pharmaceutical compositions as a medicament, particularly for use in the treatment or prophylaxis of cancers such as multiple myeloma.
Resumen de: US2025333502A1
Methods are provided to manipulate phagocytosis of cells, including hematopoietic cells, e.g. circulating hematopoietic cells, bone marrow cells, acute leukemia cells, etc.; and solid tumor cells. In some embodiments of the invention the circulating cells are hematopoietic stem cells, or hematopoietic progenitor cells, particularly in a transplantation context, where protection from phagocytosis is desirable. In other embodiments the circulating cells are leukemia cells, particularly acute myeloid leukemia (AML), where increased phagocytosis is desirable.
Resumen de: US2025332150A1
T-cell acute lymphoblastic leukemias (T-ALL) are aggressive hematological malignancies associated with poor clinical outcome. TP53 alterations (TP53Alt) were rarely identified in T-ALL at diagnosis and their prognostic impact remains unclear. In a cohort of 476 adults and pediatric T-ALL, TP53Alt were observed in 4% of cases and were associated with chemoresistance and poor prognosis. APR-246, a small compound which restores wild-type configuration to mutated p53, showed efficacy in T-ALL harboring TP53 mutations. More importantly, in TP53 germline T-ALL, Notch 1 pathway gain of function mutations were associated with substantial sensitivity to APR-246. Mechanistically, Notch 1 activation via p53 downregulation and subsequent ferroptosis induction led to preferential APR-246 sensitivity. Given that Notch 1 pathway oncogenic activation is present in more than 70% of T-ALLs, these observations pave the way for promising perspectives in T-ALL treatment which could benefit from the Achilles heel associated with Notch 1 activation sensitizing leukemia cells to APR-246-induced ferroptosis, thus extending the use of APR-246 in T-ALL beyond TP53 alterations.
Resumen de: US2025334578A1
The present invention relates to antigen binding molecules that are at least bispecific and specifically bind to CD200 and CD123 on the cellular surface of leukemic stem cells (LSCs). The present invention further relates to a method for identifying such antigen binding molecules and the use of the antigen binding molecules for the diagnosis and treatment of leukemia, such as AML or CML, and in particular pediatric forms thereof.
Resumen de: US2025333795A1
The present invention relates to a composition for amplifying a FLT3 gene, and uses thereof, and, more particularly, to a composition comprising a primer set capable of simultaneously amplifying an ITD detection region and a TKD mutation region of the FLT3 gene, and uses thereof. The composition for gene amplification, according to the present invention, enables the simultaneous performance of: diagnosis of acute myeloid leukemia (AML) in patients having FLT3-ITD mutations; determination of targeted anticancer treatment prescription for AML patients having FLT3-ITD mutations; detection of minimal residual disease (MRD) in AML patients; prognosis prediction in AML patients; and identification of drug resistance to AML tyrosine kinase inhibitors, and thus, shortens the time to derive analysis results from samples and enables efficient testing. The present invention enables the selection of correct and rapid diagnosis and treatment methods in the treatment of patients with acute myeloid leukemia, and thus is useful for early treatment and recurrence prevention.
Resumen de: US2025333421A1
The present invention relates to pharmaceutical agents useful for therapy and/or prophylaxis in a mammal, pharmaceutical composition comprising such compounds, and their use as menin/MLL protein/protein interaction inhibitors, useful for treating diseases such as cancer, including but not limited to leukemia, myelodysplastic syndrome (MDS), and myeloproiiferative neoplasms (MPN); and diabetes.
Resumen de: WO2025223509A1
Disclosed in the present invention are a class of dienyl long-chain compounds, and a preparation method therefor and the use thereof. The structure is as shown in formula I, and the definition of each substituent in the formula is as described in the description and the claims. The compound of the present invention has an ACLY inhibitory activity and a lipid synthesis inhibitory activity, and can be used in the preparation of a drug for treating metabolic diseases such as hyperlipidemia and atherosclerosis, or a variety of cancers such as lung cancer, pancreatic cancer, breast cancer, ovarian cancer, liver cancer, intestinal cancer, brain cancer and acute myeloid leukemia.
Resumen de: US2025333530A1
The present invention relates to methods of treating B-cell proliferative disorders, e.g., primary refractory or relapsed diffuse large B-cell lymphoma (DLBCL), by administering glofitamab in combination with gemcitabine and oxaliplatin. Further the invention related to an optimized corticosteroid prophylaxis for glofitamab resulting in lower incidence of cytokine release syndrome (CRS).
Resumen de: WO2024137713A1
The present disclosure relates to the use of pelabresib, and pharmaceutically acceptable salts and hydrates thereof, for treating lower risk myelodysplastic syndrome (LR-MDS) and conditions associated therewith.
Resumen de: AU2024238830A1
The present disclosed invention provides pharmaceutical compositions and methods of use for bisbenzylisoquinolines such as 6,6',7,12-tetramethoxy-2,2'-dimethyl-berbaman, and analogs, derivatives, isomers, and modified forms such as crystalline, salt forms, or a salt of this compound with a pharmaceutically acceptable acid or in combination with other agents to treat acute, chronic and pre-leukemic conditions as well as lymphomas and solid tumors. These include preneoplastic and neoplastic diseases and solid tumors including but not limited to acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myeloid leukemia (CML), atypical chronic myeloid leukemia (aCML), and acute myeloid leukemia (AML), polycythemia vera (PV), chronic lymphoblastic leukemia (CLL), myeloproliferative syndrome (MPS), myelodysplastic syndrome (MDS), myeloproliferative neoplasms (MPN), myelofibrosis (MF), and polycythemia vera (PV).
Resumen de: AU2025202444A1
TTC-018 USE OF ANTI-HA-1 AND ANTI-HA-2 BINDING PROTEINS FOR TREATMENT OF AML, ALL, AND MDS The present disclosure encompasses, among other things, methods and compositions for use in the treatment of acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL), or myelodysplastic disorder (MDS) in subjects that received HCT. The present disclosure relates, at least in part, to T cells engineered to express particular T Cell Receptors (TCRs) and their use in the treatment of acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL), or myelodysplastic disorder (MDS) in subjects that received HCT. TTC-018 USE OF ANTI-HA-1 AND ANTI-HA-2 BINDING PROTEINS FOR TREATMENT OF AML, ALL, AND MDS The present disclosure encompasses, among other things, methods and compositions for use in the treatment of acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL), or myelodysplastic disorder (MDS) in subjects that received HCT. The present disclosure relates, at least in part, to T cells engineered to express particular T Cell Receptors (TCRs) and their use in the treatment of acute myeloid leukemia (AML), acute lymphocytic leukemia (ALL), or myelodysplastic disorder (MDS) in subjects that received HCT. pr - - - - - , , p r h e p r e s e n t d i s c l o s u r e e n c o m p a s s e s , a m o n g o t h e r t h i n g s , m e t h o d s a n d c o m p o s i t i o n s f o r u s e i n t h e t r e a t m e n t o f a c u t e m y e l o i d l e u k e m i a ( ) , a c u t e l y m p h o c y t i
Nº publicación: US2025324955A1 23/10/2025
Solicitante:
VERSITECH LTD [CN]
Versitech Limited
Resumen de: US2025324955A1
Genetically modified zebrafish, in which mutation combinations frequently identified in human AML are stably expressed in the stem cell population of the fish, are provided. The combination of mutations result in morphologic, cytochemical and molecular changes of its blood cells that are remarkably similar to those in human AML. The zebrafish model provides a foundation for the study of AML initiation and progression and a high throughput in vivo drug screening platform to identify personalized therapies for AML based on specific mutation combinations. The method of drug screening includes contacting embryos or adult fish containing mutations as disclosed herein, with a test agent, at test concentrations and test intervals to determine the therapeutic effect if any, of the test agent.