Resumen de: WO2025134050A1
Embodiments of the present disclosure relate to methods of treating multiple myeloma in a subject in need thereof, comprising administering a therapeutically effective amount of a BCMA x GPRC5D x CD3 trispecific antibody or trispecific binding fragment thereof, to the subject to the subject to treat the multiple myeloma.
Resumen de: WO2025132479A1
The role of pro- and anti-inflammatory macrophages in disease depends on the specific disease and the balance between the two types of macrophages. Imbalances can lead to the development or progression of diseases, and targeting macrophage function may be a potential therapeutic approach for certain diseases. For example, by altering the phenotype and function of TAM-M2, it is possible to shift the immune response from an anti-inflammatory to a pro-inflammatory state, which may help reduce tumor progression. Here, the inventors demonstrate the ability of Gilteritinib to reprogram primary human macrophages. Gilteritinib is a targeted therapy used in the treatment of acute myeloid leukemia (AML) with a specific genetic mutation called FLT3-internal tandem duplication (FLT3-ITD) or a tyrosine kinase domain (TKD) mutation. Accordingly, the present invention relates to an FLT3 inhibitor to modulate the immune environment and enhance existing therapies by blocking immunosuppressive immune cells.
Resumen de: TW202440945A
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: KR20250095509A
본 발명은 miRNA500 억제제를 포함하는 T세포 림프종의 예방 또는 치료용 약제학적 조성물에 관한 것으로, 본 발명의 miRNA500 억제제를 포함하는 T세포 림프종의 예방 또는 치료용 약제학적 조성물은 miRNA500의 발현, 기능 또는 활성을 억제 또는 하향 조절하여 T세포 림프종에 대한 항종양 활성을 나타내므로, T세포 림프종의 예방 또는 치료 용도로 유용하게 이용될 수 있다.
Resumen de: AU2025204331A1
PHARMACEUTICAL FORMULATIONS OF BRUTON'S TYROSINE KINASE INHIBITOR Abstract Described herein are pharmaceutical formulations of Bruton's tyrosine kinase (Btk) inhibitor I-((R)-3-(4-amino-3-(4-phenoxyphenyl)-IH-pyrazolo 3,4-dpyrimidin- l-yl)piperidin-l-yl)prop-2-en-I-one. Also disclosed are methods of using the Btk inhibitor, alone or in combination with other therapeutic agents, for the treatment of autoimmune diseases or conditions, heteroimmune diseases or conditions, cancer, including lymphoma, and inflammatory diseases or conditions. PHARMACEUTICAL FORMULATIONS OF BRUTON'S TYROSINE KINASE INHIBITOR Abstract Formulation A Formulation B Formulation C Formulation D 0 6 12 18 24 Nominal Time Post-Dose (h) Described herein are pharmaceutical formulations of Bruton's tyrosine kinase (Btk) inhibitor I-((R)-3-(4-amino-3-(4-phenoxyphenyl)-IH-pyrazole 3,4-dpyrimidin- 1-yl)piperidin-l-yl)prop-2-en-I-one. Also disclosed are methods of using the Btk inhibitor, alone or in combination with other therapeutic agents, for the treatment of autoimmune diseases or conditions, heteroimmune diseases or conditions, cancer, including lymphoma, and inflammatory diseases or conditions. un ' u n b s t r a c t o r m u l a t i o n o r m u l a t i o n Mean Ibrutinib Plasma Concentration (ng/mL) o r m u l a t i o n o r m u l a t i o n o m i n a l i m e o s t - o s e ( h ) e s c r i b e d h e r e i n a r e p h a r m a c e u t i c a l f o r m u l a t i o n s o f r u t o n ' s t y r o s i n e k i n a s e (
Nº publicación: WO2025137368A1 26/06/2025
Solicitante:
CELLARITY INC [US]
CELLARITY, INC
Resumen de: WO2025137368A1
A myelodysplastic syndrome-related detection system obtains single-nucleus or single-cell transcriptome data for genes for each of a plurality of nuclei or cells. Each nucleus or cell is obtained from a sample from a different subject in a cohort. Metadata for each respective subject is obtained that indicates whether the respective subject has myelodysplastic syndrome or is healthy. The nuclei or cells are clustered into clusters by computing distances using the transcriptome data for the genes for each unique pair of nuclei or cells in the plurality of nuclei or cells and through evaluation of these distances with a criterion function. Each cluster has a subset of nuclei or cells. The metadata identifies a cluster associated with the myelodysplastic syndrome on the basis that the cluster is enriched for nuclei or cells from subjects having the myelodysplastic syndrome.