Absstract of: WO2021228956A1

The present invention relates to the treatment of cutaneous T-cell lymphomas (CTCL) and TFH derived lymphomas. In this study, the inventors showed the expression of ICOS by tumor cells in the skin of patients with MF and SS (CTCL) at different stages of the disease, and in the blood of patients with SS. The idea was thus to kill these tumor cells using ADC-antibodies specifics to ICOS. Thanks to cell lines murine xenograft models and Patient Derived Xenografts (PDXs), they showed the efficacy of such anti-ICOS ADCs on TFH-derived lymphomas, such as CTCL and AITL. Thus, the present invention relates to an anti-ICOS antibody for use in the treatment of a cutaneous T-cell lymphomas (CTCL) and/or a TFH derived lymphoma in a subject in need thereof.

Absstract of: WO2021228783A1

Methods of treating cancers using a BCMAxCD3 bispecific antibody are described.

Absstract of: EP4151653A1

Provided are a CD22-targeted chimeric antigen receptor, a preparation method therefor and an application thereof. The chimeric antigen receptor comprises a leader sequence, a CD22-targeted scFv, a hinge region, a transmembrane region, and an intracellular signal domain. Provided are a nucleic acid molecule encoding the chimeric antigen receptor and a corresponding expression vector, a CAR-T cell, and an application thereof. The chimeric antigen receptor targets CD22 positive cells and can be used for treating CD22-positive B-cell leukemia, and some CD19-negative and CD22-positive patients in which acute B-cell leukemia has recurred after anti-CD19 CAR-T treatment.

Absstract of: GB2610806A

A combination of proteins comprising a recombinant Bovine ephemeral fever virus (BEFV) glycoprotein (Gb protein) and a BEFV matrix protein (M protein). Another aspect of the invention is a composition comprising a nucleic acid encoding a recombinant BEFV glycoprotein and a nucleic acid encoding a BEFV matrix protein. The glycoprotein can have a sequence identity 90% to that of SEQ ID NO 1. The matrix protein can have a sequence identity 90% to that of SEQ ID NO 3. The nucleic acids can be operably linked to regulatory sequences. The nucleic acids can be contained in a recombinant lumpy skin disease virus (LSDV) expression vector comprising a stabilised SOD-homolog (SODis) gene. A further aspect of the invention is a vaccine comprising the combination of proteins or composition. An immunologically effective response against bovine leukaemia virus can also be induced in a subject. The subject can be a mammal (e.g. cattle or buffalo).

Absstract of: WO2021231737A1

The disclosure is directed to crystalline forms of the compound of Formula I: Formula (I), and pharmaceutically acceptable salts thereof. Pharmaceutical compositions comprising compounds of Formula I as well as methods of their use and preparation, are also described.

Absstract of: WO2023039240A1

Disclosed herein are heterocyclic compounds that inhibit the binding of KRas. Also disclosed are pharmaceutical compositions that include the compounds. Methods of using the KRas 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, lung cancer, colorectal cancer, pancreatic cancer, and other diseases or conditions dependent on KRas interaction.

Absstract of: WO2023038475A1

The present invention relates to a method for preparing directly reprogrammed natural killer (drNK) cells or chimeric antigen receptor (CAR)-gene-introduced CAR-drNK cells using a material and method for inhibiting the expression and/or function of the B-cell leukemia 11B (BCL11B) gene. The present invention also relates to: drNK cells or CAR-drNK cells prepared by a BCL11B gene-based cell reprogramming method; and a cell therapeutic agent and a composition containing same for preventing or treating cancer and infectious diseases and/or inflammatory diseases caused by viruses, bacteria, fungi, and the like.

Absstract of: US2023084899A1

The present invention relates to combinations of at least two components, component A and component B, component A being an AhR inhibitor, and component B being pembrolizumab or nivolumab. A further aspect of the present invention relates to combinations of three components, component A, component B, and component C; component A being an AhR inhibitor, component B being pembrolizumab or nivolumab, and component C being a further pharmaceutical agent. The present invention further relates to the use of such combinations as described herein for the preparation of a medicament for the treatment or prophylaxis of a disease, particularly for the treatment or prophylaxis of cancers of the breast, respiratory tract, brain, reproductive organs, digestive tract, urinary tract, eye, liver, skin, kidney, head and neck, thyroid, parathyroid, and their distant metastases, lymphomas, sarcomas and leukemias.

Absstract of: US2023079399A1

The disclosure provides compounds of Formula I, which may be useful as aldehyde de-hydrogenase inhibitors and the pharmaceutically acceptable salts thereof. The variables, J, R4, G, Q, and ring A are defined herein. Aldehyde dehydrogenase inhibitors of Formula I are useful for treating a variety of conditions including cancer and inflammation The disclosure includes methods for using compounds and salts of Formula I to treat colon cancer, pancreatic cancer, nasopharyngeal carcinoma, thyroid cancer, prostate cancer, ovarian cancer, head and neck squamous cell carcinoma, lung cancer, hepatocellular carcinoma, leukemia, brain tumorsbreast cancer, atherosclerosis, ischaemic heart disease, acne vulgaris, asthma, autoimmune diseases, autoinflammatory diseases, chronic prostatitis, glomerulonephritis, inflammatory bowel disease, pelvic inflammatory disease, reperfusion injury, rheumatoid arthritis, sarcoidosis, transplant rejection, vasculitis, and interstitial cystitis. The disclosure also includes pharmaceutical compositions containing a compound or salt of Formula I.

Absstract of: WO2023036161A1

The use of mitoxantrone liposome, bortezomib and dexamethasone in the preparation of a drug for treating multiple myeloma, a pharmaceutical composition product containing the mitoxantrone liposome, bortezomib and dexamethasone and used for treating multiple myeloma, and a method for treating multiple myeloma using the mitoxantrone liposome, bortezomib and dexamethasone. Multiple myeloma is preferably recurrent/refractory multiple myeloma. The mitoxantrone liposome is preferably mitoxantrone hydrochloride liposome.

Absstract of: AU2023200873A1

Provided herein are small molecule inhibitors of ASHIL activity and small molecules that facilitate ASH1L degradation and methods of use thereof for the treatment of disease, including acute leukemia, solid cancers and other diseases dependent on activity of ASHIL.

Absstract of: AU2022221496A1

218015-0024U Disclosed in a method of treating a myeloid neoplasm, acute leukemia, or infectious disease in a subject, the method including administering to a subject in need thereof a pegylated interferon-a at a regular interval of every 2 to 8 weeks at a first dose of 250 to 500 pg.

Absstract of: AU2021320129A1

The present disclosure relates to anti-BAFFR antibodies and binding fragments thereof, alone or in combination with additional agents, for use in the treatment of B cell malignancies, for example a B-cell non-Hodgkin's lymphoma.

Absstract of: US2023080834A1

The present invention relates to compounds that inhibit NIK and pharmaceutical compositions comprising such compounds and methods of using the same. These compounds and pharmaceutical compositions are envisaged to be useful for preventing or treating diseases such as cancer (such as B-cell malignancies including leukemias, lymphomas and myeloma), inflammatory disorders, autoimmune disorders, immunodermatologic disorders such as palmoplantar pustulosis and hidradenitis suppurativa, and metabolic disorders such as obesity and diabetes.

Absstract of: US2023077903A1

A method of treating a patient who has hepatocellular carcinoma (HCC), colorectal carcinoma (CRC), glioblastoma (GB), gastric cancer (GC), esophageal cancer, NSCLC, pancreatic cancer (PC), renal cell carcinoma (RCC), benign prostate hyperplasia (BPH), prostate cancer (PCA), ovarian cancer (OC), melanoma, breast cancer (BRCA), CLL, Merkel cell carcinoma (MCC), SCLC, Non-Hodgkin lymphoma (NHL), AML, gallbladder cancer and cholangiocarcinoma (GBC, CCC), urinary bladder cancer (UBC), and uterine cancer (UEC) includes administering to said patient a composition containing a population of activated T cells that selectively recognize cells in the patient that aberrantly express a peptide. A pharmaceutical composition contains activated T cells that selectively recognize cells in a patient that aberrantly express a peptide, and a pharmaceutically acceptable carrier, in which the T cells bind to the peptide in a complex with an MHC class I molecule, and the composition is for treating the patient who has HCC, CRC, GB, GC, esophageal cancer, NSCLC, PC, RCC, BPH, PCA, OC, melanoma, BRCA, CLL, MCC, SCLC, NHL, AML, GBC, CCC, UBC, and/or UEC. A method of treating a patient who has HCC, CRC, GB, GC, esophageal cancer, NSCLC, PC, RCC, BPH, PCA, OC, melanoma, BRCA, CLL, MCC, SCLC, NHL, AML, GBC, CCC, UBC, and/or UEC includes administering to said patient a composition comprising a peptide in the form of a pharmaceutically acceptable salt, thereby inducing a T-cell response to the HCC, CRC, GB

Absstract of: CA3130929A1

Treatment-eradicated cancer subclones have been reported in leukemia and have recently been detected in solid tumors. Here we introduce Differential Subclone Eradication and Resistance Analysis (DSER), a method developed to identify molecular targets for improved therapy by direct comparison of genomic features of eradicated and resistant subclones in pre- and post-treatment samples from a patient with BRCA2-deficient metastatic prostate cancer. FANCI and EYA4 were identified as candidate DNA repair-related targets for converting subclones from resistant to eradicable, and RNAi-mediated depletion of FANCI confirmed it as a potential target. The EYA4 alteration was associated with adjacent L1 transposon insertion during cancer evolution upon treatment, raising questions surrounding the role of therapy in L1 activation. Both carboplatin and enzalutamide turned on L1 transposon machinery in LNCaP and VCaP but not in PC-3 and 22Rv1 prostate cancer cell lines. L1 activation in LNCaP and VCaP was inhibited by the antiretroviral drug azidothymidine. L1 activation was also detected post-castration in LuCaP 77 and LuCaP 105 xenograft models and post-chemotherapy in previously published time-series transcriptomic data from SCC25 head and neck cancer cells. In conclusion DSER provides an informative intermediate step toward effective precision cancer medicine and should be tested in future studies, especially those including dramatic but temporary metastatic tumor regression. L1 transpo

Absstract of: EP4148055A1

The present disclosure relates to a crystal form of a macrocyclic tyrosine kinase inhibitor and a preparation method therefor, specifically relates to a crystal form of a compound represented by Formula (I) and a preparation method therefor, a pharmaceutical formulation and pharmaceutical composition containing the crystal form, and an application thereof in preparing drugs for treating and/or preventing pain, inflammation, cancer, neurodegenerative diseases, and autoimmune diseases mediated by one or more tyrosine kinase receptors in a tropomyosin receptor kinase (TRK), an anaplastic lymphoma kinase (ALK) and/or a c-ros oncogene 1 receptor kinase (ROS1).

Absstract of: WO2023033638A1

The present invention relates to an indole alkaloid, specifically the alkaloid (33,3aR,8aS)-3-butyl-5-hydroxy-3,3a,8a-trimethyl-3,3a,8,8a-tetrahydro-2H-furo[2,3-b] indole-2-one, with the generic name Andranone, as an antineoplastic agent against neoplastic cells of colon cancer, breast cancer, leukaemia, central nervous system cancer, prostate cancer, lung cancer and cervical cancer.

Absstract of: WO2023029833A1

An SOS1 inhibitor, and a preparation method therefor and the use thereof. The SOS1 inhibitor has a structural formula as represented by formula (I), wherein the symbols and variables are as defined in the description. The SOS1 inhibitor has an SOS1 inhibitory activity and can be used for treating diseases, such as head and neck cancer, lung cancer, mediastinal tumors, gastrointestinal tumors, prostate cancer, testicular cancer, gynecological tumor, breast cancer, kidney and bladder cancer, endocrine system tumor, soft tissue sarcoma, osteosarcoma, rhabdoid tumors, mesothelioma, skin cancer, peripheral nervous system tumors, central nervous system tumors, lymphoma, leukemia, unknown primary cancer, Noonan syndrome, cardiofaciocutaneous syndrome, hereditary gingival fibromatosis and related syndromes thereof.

Absstract of: WO2023030437A1

The present disclosure provides a use of a PI3K inhibitor and a BTK inhibitor in the preparation of a drug for treating lymphoma. Specifically, in the present disclosure, P13K inhibitor is selected from a compound represented by formula (I) or a pharmaceutically acceptable salt thereof, and a BTK inhibitor is selected from a compound represented by formula (II) or a pharmaceutically acceptable salt thereof.

Absstract of: US2023073558A1

Aspects of the disclosure relate to compositions and methods for predicting prognosis and classifying risk of subjects having certain cancers, for example acute myeloid leukemia (AML). In some embodiments, methods described by the disclosure comprise a step of assessing the mRNA expression of certain leukemic stem cell (LSC)-enriched genes in a subject to produce a predictive score for pediatric AML. In some embodiments, methods described by the disclosure comprise a step of assessing the mRNA expression of certain genes of pharmacological relevance for standard chemotherapy consisting of Cytarabine (also known as Ara-C), daunorubicin and etoposide in a subject to produce a predictive score for pediatric AML.

Absstract of: US2023076866A1

The present application discloses a human T-lymphoblastic leukemia/lymphoma cell strain named as ZYXY-T1, and its construction method and use thereof. It was conserved in China Center for Type Culture Collection (Wuhan, China) on Jan. 20, 2021, and the preservation number was CCTCC NO: C202143. The present application is obtained by separating mononuclear cells from peripheral blood of one ETP-ALL patient, and culturing the cells in vitro for continuous natural passage. The strain has the typical surface antigen expression characteristics of ETP-ALL, that is, it does not express CD1α, CD5 or CD8, and highly expresses a stem cell marker CD34, and has good proliferation ability in vitro and tumorigenesis ability in vivo; it can be used as a cell material to study the occurrence and development mechanism of ETP-ALL, and can also be used to screen and evaluate ETP-ALL drugs to guide clinical medication.

Absstract of: US2023073499A1

The present invention belongs to the field of cancer therapy and relates to a composition or product comprising at least one retinoid compound, at least one arsenic compound and at least one proteasome inhibitor, for use in the treatment of acute myeloid leukemia (AML) where the tumor cells are positive for the FLT3-ITD mutation.

Absstract of: WO2023031403A1

The present invention relates to anti-CD25 antibodies for use in the treatment of acute myeloid leukemia (AML) and diffuse large B-cell lymphoma (DLBCL).

Absstract of: US2023071910A1

Provided herein are methods of administering a dose of T cells for treating subjects with indolent non-Hodgkin3 s lymphoma (NHL), and related methods, compositions, uses and articles of manufacture. The cells express a recombinant receptor such as a chimeric antigen receptor (CAR) for targeting an antigen of the lymphoma, such as CD19. In some embodiments, the methods are for treating grade 1-3 A follicular lymphoma (FL 1-3 A) or marginal zone lymphoma (MZL), including in heavily pretreated or poor-prognosis subjects, such as subjects that have relapsed after treatment with, or are refractory to treatment with, one or more prior therapies.