83 results about "Solid cancer" patented technology

Provided is a method for treating solid cancer using an anti-CD47 antibody.

There is provided a positron-emitting radionuclide labelled peptide for non-invasive PET imaging of the Urokinase-type Plasminogen Activator Receptor (uPAR) in humans. More specifically the invention relates to human uPAR PET imaging of any solid cancer disease for diagnosis, staging, treatment monitoring and especially as an imaging biomarker for predicting prognosis, progression and recurrence.

This article provides information on multi-chain chimeric peptides and their use in the treatment of unresectable, advanced, recurrent and / or metastatic solid tumors or unresectable, advanced, recurrent and / or metastatic solid cancers.

An injectable liquid containing bioactive molecules released from a powder comprising a neo-synthesized extracellular matrix for use in the treatment or prevention of cancer, in particular in the local treatment of solid tumors.

The present disclosure provides a group of aromatic (e.g., pyridinyl, pyrimidinyl, pyrazinyl, or phenyl) diamidine analogs and pharmaceutically acceptable salts that are useful for treating a proliferative disease. The proliferative disease may include solid cancer or blood cancer. Compositions, methods of synthesizing the same and methods for treating various cancer using the analogs are disclosed herein. The present disclosure also provides pharmaceutical formulations comprising at least one of the compounds with a pharmaceutically acceptable carrier, diluent or excipient therefor.

To provide a therapeutic agent for PARP inhibitor-resistant cancer.SOLUTION: The present invention relates to a pharmaceutical composition for treating or preventing a solid cancer patient having resistance to a PARP inhibitor, and the pharmaceutical composition according to the present invention can effectively reduce the size of a tumor in a patient having resistance to a PARP inhibitor.SELECTED DRAWING: Figure 4

Methods of improving PD-1 based immunotherapy in a subject suffering from a solid cancer, comprising decreasing bone morphogenetic protein 1 (BMP1) levels or function in T cells or in a tumor microenvironment (TME) or extracellular matrix (ECM) of the solid cancer are provided. Methods of treating a solid cancer comprising administering a PD-1 based immunotherapy and decreasing BMP1 levels or function in T cells or a TME or ECM of the solid cancer are also provided. Antibody drug conjugates comprising an anti-PDl blocking antibody and a BMP1 inhibiting small molecule or antibody or antigen binding fragment thereof small molecule inhibitor and pharmaceutical compositions for use in the methods of the invention are also provided.

The present invention provides a use of paclitaxel cationic liposomes in the manufacture of a medicament for treating terminal solid cancer, a use of paclitaxel cationic liposomes and a systemic therapeutic agent in the manufacture of a medicament for treating terminal solid cancer, and a method for treating terminal solid cancer, in which a therapeutically effective amount of paclitaxel cationic liposomes is administered to a patient with terminal solid cancer, or a therapeutically effective amount of paclitaxel cationic liposomes and a systemic therapeutic agent is administered to a patient with terminal solid cancer.

Provided is a method for treating solid cancer using an anti-CD47 antibody.

The present invention relates to a use of a substance comprising point-mutated FoxM1 protein and peptide for inhibiting growth, migration and invasion of cancer cells. In addition, it relates to a use of a substance comprising point-mutated FoxM1 protein and peptide for inhibiting malignancy in a tumor microenvironment by inhibiting polarization into tumor-associated macrophages in a tumor microenvironment. It relates to a use as an apoptotic inducer using the action of sensitively inhibiting cancer cell death in metastatic cancer cells as well as general solid cancers.

The present invention relates to a pharmaceutical composition for prevention or treatment of solid cancer comprising an epidithiodioxopiperazine derivative compound based on a parent structure comprising an intramolecular disulfide bridge in an epidithiodioxopiperazine ring or a pharmaceutically acceptable salt thereof as an active ingredient.

The present disclosure provides a group of aromatic (e.g., pyridinyl, pyrimidinyl, pyrazinyl, or phenyl) diamidine analogs and pharmaceutically acceptable salts that are useful for treating a proliferative disease. The proliferative disease may include solid cancer or blood cancer. Compositions, methods of synthesizing the same and methods for treating various cancer using the analogs are disclosed herein. The present disclosure also provides pharmaceutical formulations comprising at least one of the compounds with a pharmaceutically acceptable carrier, diluent or excipient therefor.

The present disclosure provides methods, compositions, uses, and kits for treatment of solid cancer (e.g., urothelial cancer (UC), head and neck squamous cell carcinoma (HNSCC), cervical cancer (CC), endometrial carcinoma (EC), or triple-negative breast cancer (TNBC)) using anti-human Nectin-4 therapeutics.

Provided is a means to predict the anticancer therapeutic efficacy of 1-((5-(1R)-1-fluoroethyl)-1,3,4-oxadiazol-yl)methyl)-6-(4-methoxypyrrolo[2,1-f][1,2,4]triazin-5-yl)-2-methyl-1H-imidazo[4,5-b]pyridine or a derivative thereof in solid cancer and thereby specifying a subject who will be the most benefitted from treatment with the compound and treatment with the compound in combination with another drug and / or another therapy. As a biomarker for predicting therapeutic response to the compound, a genetic character predicted to impart sensitivity to CLK inhibition is used.

The present invention relates to the treatment of diseases associated with inflammation including solid cancers. More particularly, certain methods relate to the administration (e.g., intravenously) of polyhedrin protein (PODS) crystals for the delivery of one or more therapeutic proteins. This enables targeted release of low doses of the therapeutic protein at sites of the disease.

The present invention consists in combining low dose intestinal radiation (ILDR) with immunotherapy or other antineoplastic treatments, in the ideal context of intestinal presence or prevalence of Christensenellaceae family members, especially for solid cancers at an advanced stage (refractory to first line chemo or immunotherapy). The invention also pertains to a bacterial composition,e.g. comprising Chistensenella bacteria, for use in the treatment of cancer in a patient, in combination with intestinal low dose radiotherapy (ILDR) and an antineoplastic treatment.

The invention provides improved compositions and methods for the treatment of solid cancers.

Disclosed herein are methods and compositions for inhibiting the interaction of a multiple endocrine cancer suppressor protein with an MLL protein. In particular, the present application provides compositions and methods for inhibiting the interaction of multiple endocrine cancer suppressor proteins with MLL1, MLL2, and MLL-fusion cancer proteins. The compositions and methods of use are useful for the treatment of leukemia, solid cancers, diabetes and other diseases that depend on MLL1, MLL2, MLL fusion protein and / or multiple endocrine cancer suppressor protein activity.

The present disclosure provides compositions and methods of use to inhibit the interaction of menin with MLL1, MLL2 and MLL-fusion oncoproteins. The compositions and methods of use are useful for the treatment of leukemia, solid cancers, diabetes and other diseases dependent on activity of MLL1, MLL2, MLL fusion proteins, and / or menin.

Disclosed herein are methods of diagnosing severity, aggressiveness, or prognosis of a solid cancer by determining if miR-155 is overexpressed. Also disclosed herein are methods of treating, preventing, decreasing, eliminating, and / or ameliorating a cancer by synthetic nucleic acids encoding administering inducible T-cell costimulatory ligand (ICOSL) and / or RELA, thereby upregulating ICOSL and MHC-I on cancerous cells to improve the efficacy of immune cell therapies and checkpoint inhibitors. Any of the disclosed methods can further be paired with administration of an miR-155 inhibitor (e.g., cobomarsen).

A room temperature injectable thermo-responsive hydrogel comprises a P407 poloxamer base hydrogel, chitosan, 2-Hydroxypropyl ß-cyclodextrin. and genipin. The chitosan and genipin form an interpenetrating scaffold within the hydrogel in which the chitosan is crosslinked with genipin. Chemotherapeutic drugs can be added to the hydrogel singly or in combination in effective amounts without any loss of thermo-responsiveness in the hydrogel. Therapeutic use of the thermo-responsive hydrogel in the intratumoural treatment of solid cancer is also described.

The present invention relates to a bispecific antibody fragment in which a nanobody specifically binding to EpCAM is connected by a flexible peptide linker ((GGGGS)n) to a single-chain antibody fragment (scFv) specifically binding to CD3, and is an antibody platform technology for anticancer therapy, wherein a selective point mutation is introduced into the antigen-binding site (CDR) of the antibody, thereby modulating binding affinity for an antigen and immunological safety. The design is such that the EpCAM-binding domain has maximized accessibility and selective binding ability to solid cancer cells by having utilized a nanobody having excellent tissue penetration, and the CD3-binding domain can inhibit T-cell overactivation and immunotoxicity (CRS) by having utilized scFv, the affinity of which can be modulated based on the therapeutic purpose. In particular, the affinity of antibody fragments to EpCAM and CD3 antigens is stably maintained or improved even under weakly acidic conditions (pH 5.6 to 6.7) of the tumor microenvironment, indicating that the antibody fragments can exhibit excellent anticancer effects even in solid cancer environments.

The present invention relates to the adoptive therapy using notably CAR-T cells. Here the inventors used a lentiviral vector approach to silence RINF expression in a shRNA-dependent manner and evaluate the consequences of RINF silencing on human CAR-T cells proliferation ex vivo and their functionality and capacity to eradicate tumor cells in vivo. More, the proposed methodology to improve CAR-T cells persistence and efficacy by disrupting RINF / CXXC5 is not restricted to patients suffering from hematological or solid cancers (anti-CD19, anti-EGFR, anti-BCMA . . . ) but could be also used to improve the efficacy of ACT in non-cancer diseases by such as lupus (1), cardiac fibrosis (2) or aging related-disorders (3). Thus, the present invention relates to an immune cell characterized in that it is defective for RINF.

Provided is a means to predict the anticancer therapeutic efficacy of 1-((5-(1R)-1-fluoroethyl)-1,3,4-oxadiazol-yl)methyl)-6-(4-methoxypyrrolo[2,1-f][1,2,4]triazin-5-yl)-2-methyl-1H-imidazo[4,5-b]pyridine or a derivative thereof in solid cancer and thereby specifying a subject who will be the most benefitted from treatment with the compound and treatment with the compound in combination with another drug and / or another therapy. As a biomarker for predicting therapeutic response to the compound, a genetic character predicted to impart sensitivity to CLK inhibition is used.

An anticancer agent for solid cancer contains, as an active ingredient, human parainfluenza virus type 2 expressing: at least one kind of cytokine selected from the group consisting of IL-2, IL-7, IL-12, IL-15, and IL-18; or a combination of the cytokine and CCL 19 and / or CCL21; or a mutant of either the cytokine or the combination, the mutant having the same function.

Methods, dosage regimens, and administration of antibody drug conjugates (ADCs) for the treatment of cancer are provided. More specifically, the cancer is an advanced or metastatic solid cancer.

The disclosure describes antibodies chimeric antigen receptors (CARs), CAR T cell therapeutics, and their use in treating solid cancers. In particular, the disclosure describes antibodies and CAR T constructs that bind to NRCAM in variety of solid tumors.

The present invention is directed to a method for treating solid cancer in patients with clonal hematopoiesis of indeterminate potential (CHIP). The method introduces a therapeutic intervention of dapansutrile to improve the treatment of a solid cancer, such as breast cancer, in a CHIP patient. The method includes first determining whether a patient has a CHIP condition by detecting the presence or absence of Tet2 or DNMT3A mutation from a biological sample of the patient, and then followed by a therapeutic intervention with dapansutrile in patients having a CHIP condition. This application shows a role for CHIP in driving breast cancer. The data provide a rationale for Tet2 or DNMT3A mutation screening in breast cancer patients and offer dapansutrile as a therapeutic treatment.

The present invention relates to novel pyrrolotriazine derivatives and their use as inhibitors of YES1 kinase and transcription enhancer associated domain (TEAD) activity. The compounds of the present invention effectively inhibit the activity of YES1 kinase and TEAD and are therefore useful in the prevention or treatment of YES1 kinase related diseases and TEAD related diseases, in particular solid cancers.

The present disclosure relates to methods of treating or preventing cancer (e.g., advanced solid cancer) using Compound Number 1: (Compound Number 1) or a pharmaceutically acceptable salt thereof. The disclosure also relates to pharmaceutical compositions and pharmaceutical kits suitable for treatment or prevention. (Compound Number 1)