26 results about "Solid Neoplasm" patented technology

The present disclosure is concerned with compounds and compositions for use in the prevention and treatment of cancer associated with FBOX21 mediated p85a ubiquitination such as, for example, cancer (e.g., sarcoma, a carcinoma, a hematological cancer, a solid tumor, breast cancer, cervical cancer, gastrointestinal cancer, colorectal cancer, brain cancer, skin cancer, prostate cancer, ovarian cancer, thyroid cancer, testicular cancer, pancreatic cancer, liver cancer, endometrial cancer, melanoma, a glioma, leukemia, lymphoma, chronic myeloproliferative disorder, myelodysplastic syndrome, myeloproliferative neoplasm, non-small cell lung carcinoma, renal cancer, lung cancer, colon cancer, cervical cancer, and plasma cell neoplasm (myeloma)). This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention.

GD2 specific chimeric antigen receptor effector cells for the treatment of solid tumors, possibly in combination with an enhancer of a Zeste homolog 2 (EZH2) inhibitor. The invention relates to a GD2-specific chimeric antigen receptor (GD2. CAR) effector cell for use in the treatment of solid tumors, in particular in the treatment of extracranial GD2 + tumors, such as soft tissue sarcoma and osteosarcoma, neuroblastoma, melanoma, lung cancer, bladder cancer and retinoblastoma, and brain tumors. In addition, the present invention also relates to the use of the GD2. CAR genetically modified effector cell in combination with an enhancer of a Zeste homolog 2 (EZH2) inhibitor for the treatment of solid tumors.

This invention discloses an engineered CAR-T cell targeting HIF-1α and its application in tumor immunotherapy. The CAR-T cell expresses a chimeric antigen receptor regulated by the hypoxia-responsive element HRE promoter, with its extracellular domain specifically binding to HIF-1α and its intracellular domain employing the 4-1BB+CD3ζ signaling module. Simultaneously, through immune checkpoint knockout and cytokine / chemokine modification, it achieves hypoxia-dependent activation, anti-exhaustion, high infiltration, and strong killing effects. The CAR-T cells of this invention significantly improve the adaptability to the solid tumor microenvironment and therapeutic efficacy, reduce off-target toxicity, and can be used to prepare drugs for treating malignant tumors such as lung cancer, liver cancer, pancreatic cancer, colorectal cancer, and glioblastoma, possessing significant clinical translational value.

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.

This invention discloses a class of 2-(2-(quinolin-4-yloxy)ethyl)pyridazine-3(2H)-one compounds, their preparation methods, and applications. The structure of these compounds is shown in general formula (I). This invention also discloses that the above compounds have a significant inhibitory effect on interleukin-1 receptor-associated kinase 1 (IRAK1). These compounds can inhibit the proliferation of various tumor cells, including liver cancer, lung cancer, pancreatic cancer, gastric cancer, kidney cancer, colon cancer, esophageal cancer, glioblastoma, leukemia, multiple myeloma, and other solid tumors and hematological malignancies. This invention provides a new option for tumor treatment.

Disclosed in the present invention are a PIM kinase inhibitor as shown in general formula II, a pharmaceutical composition thereof, a preparation method therefor and the use thereof in the preparation of a drug for preventing and / or treating indications related to a PIM signaling pathway. The compound of the present invention is an ideal PIM kinase inhibitor with a high activity, which can be used for treating and / or preventing diseases including autoimmune diseases and tumors, e.g., inflammatory bowel disease, hematologic malignancies such as acute myeloid leukemia, myelofibrosis and chronic lymphocytic leukemia, and solid tumors such as gastric cancer and prostate cancer.

The present application relates to the technical field of biological medicine, and particularly relates to application of fullerenol in preparation of tumor prevention or treatment drugs for inducing trained immunity. The present application finds that fullerenol can induce formation of trained immunity, activate immune reprogramming of bone marrow hematopoietic stem cells, produce long-term pro-inflammatory phenotype, form persistent immune memory, and further enhance functions of innate immune cells. It is verified by experiments that fullerenol can significantly inhibit tumor growth in an animal model without obvious systemic toxicity; epigenetic remodeling of bone marrow hematopoietic stem cells can be sustained for several weeks to several months, and has long-acting anti-recurrence potential. In addition, trained immunity induced by fullerenol can be used for immune regulation of various solid tumors, and fullerenol is simple in synthesis, can be produced on a large scale, has excellent biocompatibility and stability. Therefore, the present application has wide application prospect.

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 invention relates to application of HDAC (histone deacetylase) inhibitor and Cathepsin B inhibitor combined medicine in lung cancer treatment, and belongs to the technical field of biological medicine. Research finds that histone deacetylase inhibitors (HDAC inhibitors, HDACIs) can promote invasion and migration of tumor cells by inducing epithelial-mesenchymal transition while inhibiting tumor growth, and side effects are generated. Therefore, in order to inhibit the side effect and enable the HDAC inhibitor to effectively exert the curative effect clinically, the invention provides a novel medicine combination mode, the HDAC inhibitor and the Cathepsin B inhibitor are combined for use, so that the antitumor activity of the HDAC inhibitor is retained, the tumor invasion and migration capability induced by the HDAC inhibitor is effectively inhibited, and the curative effect of the HDAC inhibitor is effectively exerted clinically. A new strategy is provided for precise treatment of solid tumors, and the method is verified in treatment of lung cancer.

The present disclosure relates to compounds, pharmaceutical compositions, and methods of using the compounds and compositions to restore activity of von Hippel Lindau tumor suppressor protein (pVHL). Such compounds and compositions can be useful in, for example, the treatment of cancer (e.g.. a sarcoma, a carcinoma, a head-and-neck cancer, hematological cancer, a solid tumor, breast cancer, cervical cancer, gastrointestinal cancer, colorectal cancer, brain cancer, skin cancer, prostate cancer, ovarian cancer, thyroid cancer, testicular cancer, pancreatic cancer, liver cancer, endometrial cancer, melanoma, a glioma, leukemia, lymphoma, chronic myeloproliferative disorder, myelodysplastic syndrome, myeloproliferative neoplasm, non-small cell lung carcinoma, small cell lung carcinoma, renal cancer, lung cancer, colon cancer, cervical cancer, and plasma cell neoplasm (myeloma)) and von Hippel-Lindau disease (VHLD). This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention.

Disclosed herein are crystalline polymorphs of indotecan (LMP400) that can be used in the treatment of cancers associated with dysregulation of Topl and / or MYC activity, such as, for example, a sarcoma, (e.g., Ewing's sarcoma), a carcinoma, a hematological cancer, a solid tumor, breast cancer, cervical cancer, gastrointestinal cancer, colorectal cancer, brain cancer, skin cancer, prostate cancer, ovarian cancer, non-small cell lung carcinoma, thyroid cancer, testicular cancer, pancreatic cancer, liver cancer, endometrial cancer, a melanoma, a. glioma, leukemia, a lymphoma, chronic myeloproliferative disorder, myelodysplastic syndrome, myeloproliferative neoplasm, and plasma cell neoplasm (myeloma). This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention.

The invention belongs to the technical field of tumor molecule detection, and particularly discloses a method and a kit for detecting HER2 gene mRNA (messenger Ribonucleic Acid) trace expression based on an RT-ddPCR (Reverse Transcription-Derived Polymerase Chain Reaction) technology. The kit contains a cross HER2 exon 19-20 / 20-21 specific primer probe, a reference gene specific primer probe and reverse transcriptase, and the ddPCR premix solution, the HER2 probe and the reference gene probe are respectively marked with different fluorophores. According to the detection method, after RNA extraction, reverse transcription and RT-ddPCR amplification of a detection sample are carried out, the HER2 / internal reference copy number ratio is calculated to realize typing, a breast cancer sample is completely negative when the Ratio is smaller than 1.0, is ultralow in expression when the Ratio is larger than or equal to 1.0 and smaller than 5.0, is low in expression when the Ratio is larger than or equal to 5.0 and smaller than 50.0, and is medium-high in expression when the Ratio is larger than or equal to 50.0. The detection sensitivity reaches 0.1 copy / microliter, absolute quantification can be achieved, adaptability to FFPE samples is high, breast cancer patients with ultralow expression of HER2 in IHC 0 can be accurately screened, a molecular basis is provided for accurate medication of ADC drugs such as Trastuzumab deruxtecan, and the kit can also be used for related detection of solid tumors such as gastric cancer and cervical cancer with HER2 gene amplification as a marker.

Disclosed herein are crystalline polymorphs of LMP744 that can be used in the treatment of cancers associated with dysregulation of Top1 and / or MYC activity, such as, for example, a sarcoma, (e.g., Ewing's sarcoma), a carcinoma, a hematological cancer, a solid tumor, breast cancer, cervical cancer, gastrointestinal cancer, colorectal cancer, brain cancer, skin cancer, prostate cancer, ovarian cancer, non-small cell lung carcinoma, thyroid cancer, testicular cancer, pancreatic cancer, liver cancer, endometrial cancer, a melanoma, a glioma, leukemia, a lymphoma, chronic myeloproliferative disorder, myelodysplastic syndrome, myeloproliferative neoplasm, and plasma cell neoplasm (myeloma). This abstract is intended as a scanning tool for purposes of searching m the particular art and is not intended to be limiting of the present invention.

The invention relates to an application of a medicine in treating tumor diseases. Specifically, the invention provides the application of the bioactive substance conjugate shown in the formula (I) in the treatment of tumor diseases, and the tumor diseases are particularly preferably used for treating local advanced or metastatic solid tumors which are difficult to treat and cannot be resected by surgery according to the existing standard. Comprise but are not limited to breast cancer, stomach cancer, lung cancer, ovarian cancer, urothelial cancer, esophageal cancer, liver cancer, colorectal cancer, cervical cancer, endometrial cancer, pancreatic cancer and brain tumor.

The invention discloses a dihydropyrazole EFTUD2 degradation agent as well as a preparation method and application thereof, the dihydropyrazole EFTUD2 degradation agent provided by the invention is designed by adopting a proteolysis targeting chimera, and a dihydropyrazole derivative is used as an EFTUD2 protein binding ligand and is connected with an E3 ubiquitin ligase ligand through connecting chains with different lengths and types. The compound has a remarkable EFTUD2 protein degradation effect, can effectively inhibit proliferation of tumor cells such as non-small cell lung cancer and the like, and also has potential treatment value on other types of solid tumors such as breast cancer, ovarian cancer, prostatic cancer and the like and blood system tumors. The synthesis route of the compound is simple and efficient, raw materials are easy to obtain, the yield is high, and the compound has a good industrialization prospect.

Aspects of this invention are related to the use of N-desmethyl ruboxistaurin and pharmaceutically acceptable formulations thereof to modulate CDK4 / 6 signaling. The invention encompasses methods for administering N-desmethyl ruboxistaurin to subjects in need, particularly those with a history of cancer or currently experiencing breast cancer, liposarcoma, lung cancer, glioblastoma, melanoma, pancreatic cancer, prostate cancer, colon cancer, ovarian cancer, colorectal cancer, bladder cancer, hepatocellular carcinoma, osteosarcoma, germ cell tumors, advanced solid tumors, lymphoma, leukemia and other hematologic malignancies. The disclosed methods extend beyond disease treatment, including supportive care during radiation chemotherapy and prevention of cancer relapse. N-desmethyl ruboxistaurin administration, alone or in combination with other cancer therapies, is effective in modulating CDK4 / 6 signaling while mitigating toxicity associated with other treatments.

The application belongs to the technical field of biological medicine, and particularly relates to a method for enhancing CIK cell activity and application thereof in tumor treatment. The method separates exosomes (particle size 50-150 nm, expressing TSG101 and Alix, not expressing CD9 and Calnexin) from CIK cell culture supernatant by ultracentrifugation, and reinfuses the exosomes at a proportion of 100-500 ug exosomes per 2x10 7 CIK cells. The exosomes can significantly improve the expression level of CIK cell IFN-gamma, promote PBMC proliferation, and in a liver cancer mouse model, it is proved that the tumor inhibition rate (70.7%) of the combination group (2x10 7 CIK cells+400 ug exosomes) is significantly better than that of the single treatment group. The application uses waste exosome resources to safely enhance the anti-tumor activity of CIK cells, and is suitable for the treatment of liver cancer, lung cancer, breast cancer and other solid tumors and hematological tumors.

The present disclosure is concerned with compounds that restore p53 activity and methods of using the compounds in the treatment of various disorders related to loss of p53 activity such as, for example, cancer (e.g., a sarcoma, a carcinoma, a head-and-neck cancer, hematological cancer, a solid tumor, breast cancer, cervical cancer, gastrointestinal cancer, colorectal cancer, brain cancer, skin cancer, prostate cancer, ovarian cancer, thyroid cancer, testicular cancer, pancreatic cancer, liver cancer, endometrial cancer, melanoma, a glioma, leukemia, lymphoma, chronic myeloproliferative disorder, myelodysplastic syndrome, myeloproliferative neoplasm, non-small cell lung carcinoma, small cell lung carcinoma, renal cancer, lung cancer, colon cancer, cervical cancer, and plasma cell neoplasm (myeloma)). This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention.

The present disclosure relates to compounds that restore p53 activity and methods of using the compounds in the treatment of various conditions associated with loss of p53 activity, such as cancer, e.g., cancer. Such as sarcoma, epithelial cancer, head and neck cancer, hematological cancer, solid tumor, breast cancer, cervical cancer, gastrointestinal cancer, colorectal cancer, brain cancer, skin cancer, prostate cancer, ovarian cancer, thyroid cancer, testicular cancer, pancreatic cancer, liver cancer, endometrial cancer, melanoma, glioma, leukemia, lymphoma, chronic myeloproliferative disease, myelodysplastic syndrome, myeloproliferative tumor, and the like; , non-small cell lung cancer, small cell lung cancer, kidney cancer, lung cancer, colon cancer, cervical cancer, and plasma cell tumor (myeloma). This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention.

The present disclosure is concerned with substituted quinazoline-2,4-diamines and compositions for the treatment of disorders associated with altered expression of SMARCA2 and / or SMARCA4 such as, for example, cancer (e.g., sarcomas, carcinomas, hematological cancers, solid tumors, breast cancer, cervical cancer, gastrointestinal cancer, colorectal cancer, brain cancer, skin cancer, prostate cancer, ovarian cancer, thyroid cancer, testicular cancer, pancreatic cancer, liver cancer, endometrial cancer, melanoma, gliomas, leukemia, lymphoma, chronic myeloproliferative disorders, myelodysplastic syndrome, myeloproliferative neoplasm, non-small cell lung carcinoma, plasma cell neoplasm (myeloma)). This abstract is intended as a scanning tool for purposes of searching in the particular art and is not intended to be limiting of the present invention.

The invention provides a novel compound I-1 and a complex or pharmaceutically acceptable salt thereof, and the compound can be used for treating various solid tumors, such as breast cancer, gastric cancer, prostate cancer, liver cancer, pancreatic cancer, cervical cancer, ovarian cancer and the like, and especially has a remarkable inhibition effect on triple-negative breast cancer.

An oncolytic virus for use in a method of treating or preventing cutaneous squamous cell carcinoma (CSCC), renal cell carcinoma (RCC), non-small cell lung cancer (NSCLC), triple negative breast cancer (TNBC), small cell lung cancer (SCLC), advanced recurrent head and neck cancer, squamous cell carcinoma of the head and neck (SCCHN), nasopharyngeal carcinoma (NPC), hepatocellular carcinoma (HCC), anal cancer, colorectal cancer (CRC), basal cell carcinoma (BCC), Merkel cell carcinoma, appendiceal carcinoma, sarcoma of the skin, recurrent melanoma after surgery, advanced or metastatic urothelial carcinoma, liver metastases, microsatellite instability high cancer (MSI-H), mixed advanced solid tumors, virally caused cancer, locoregionally advanced cancer, pediatric cancer, cancer in patients with no or minimal pre-existing anti-cancer immunity, cancer as first line therapy, cancer in previously treated patients, cancer in patients who have not received checkpoint blockade therapy, and / or cancer in patients who have received checkpoint blockade therapy, wherein the oncolytic virus: is, or is derived from, a clinical isolate which has been selected by comparing the abilities of a panel of three or more clinical isolates of the same viral species to kill tumor cells of two or more tumor cell lines in vitro and selecting a clinical isolate which is capable of killing cells of two or more tumor cell lines more rapidly and / or at a lower dose in vitro than one or more of the other clinical isolates in the panel; comprises (i) a fusogenic protein-encoding gene; and (ii) an immune stimulatory molecule or an immune stimulatory molecule-encoding gene; comprises (i) a GM-CSF-encoding gene; and (ii) an immune co-stimulatory pathway activating molecule or an immune co-stimulatory pathway activating molecule-encoding gene; and / or comprises a gene encoding a CTLA-4 inhibitor.

The application provides a compound with a structure shown in a general formula (I), a deuterium compound, a stereoisomer or a pharmaceutically acceptable salt thereof, a pharmaceutical composition containing the same and a use thereof. The compound provided by the application has a good PIM kinase inhibition effect, is a novel, high-activity and low-toxicity ideal PIM inhibitor, and can be used for treating and / or preventing diseases such as acute myeloid leukemia, myelofibrosis, chronic lymphocytic leukemia, blood tumors such as gastric cancer and prostate cancer, and solid tumors.

Disclosed herein are compounds, compositions, and methods for treating cell proliferative diseases and disorders based on present inventors discovery that Pleckstrin-2 (Plek2) can be targeted to treat cell proliferative diseases and disorders. The compositions and methods disclosed herein include or utilize the disclosed compounds as therapeutic agents which inhibit the biological activity or expression of Pleckstrin-2 (Plek2) and collectively may be referred to as “Plek2 inhibitors.” Disclosed are small molecule inhibitors of Plek2 biological activity. The compositions and method may be utilized for treating cell proliferative diseases and disorders that are characterized by elevated levels of Plek2 expression and / or by activation of the phosphatidylinositide 3-kinase (PI3K) / Akt pathway. Cell proliferative diseases and disorders that may be treated using the disclosed compositions and methods may include, but not limited to, myeloproliferative neoplasms (MPNs) such as Philadelphia (Ph)-negative MPNs, and cancers such as acute myeloid leukemia (AML) and cancers characterized by solid tumors.

The present invention relates to the use of a KRAS inhibitor (ERAS-4001) in combination with a PD-1 or PD-L1 inhibitor for treating cancer, specifically solid tumours.