45 results about "Therapeutic targeting" patented technology

In various embodiments human anti-CD46 antibodies that are internalizing and enter tumor cells via the macropinocytosis pathway are provided, as well as antibody-drug conjugates (ADCs) developed from these antibodies for diagnostic and / or therapeutic targeting of CD46-overexpressing tumors.

Breast cancer (BC) affects more than 2 million women and is the leading cause of cancer death in women worldwide. The aim of the present study was to determine whether the JNK / c-Jun pathway was involved in GR-mediated OCDO mitogenic activity and to explore the therapeutic targeting of this pathway in TNBC. The Inventors showed that the targeting of JNK1 in TNBC is essential to inhibit the mitogenic activity of OCDO. Accordingly, the present invention relates to a method of treating a subject suffering from breast cancer comprising administering to said subject a therapeutically effective amount of a JNK-1 inhibitor.

The present invention provides methods of treating ischemic and traumatic central nervous system injury by administering an antagonist of the interaction between CD47 and SIRPa. Also provided are method of increasing efferocytosis after a traumatic or ischemic CNS injury by administering an antagonist of the interaction between CD47 and SIRPa.

The present invention relates to methods, uses, and compositions for the treatment of cancer (e.g., a breast cancer or a pancreatic cancer). More specifically, the invention concerns the treatment of patients having cancer for the therapeutic inhibition of cancer cell growth and metastasis with an anti-Cadherin 11 monoclonal antibody with specific monoclonal antibody clones 23C6 or 3H10.

Metastasis is a major cause of fatality and expense in cancer. Many metastatic patients express calcified, fibrotic, or deep-seated (lymph / Jung / brain) lesions that are not easily profiled. For such patients, decision-making regarding treatment selection is population-based and heavily reliant on standards of care and are not tailored to the individual's tumor. The present disclosure provides methods of identifying treatment protocols for cancer patients using released tumor cells (RTCs). Method described herein include isolating / enriching RTCs, profiling RTCs and comparing RTCs to reference RTC profile libraries.

The present invention discloses a method of using the said inhibitors for the treatment and / or prevention of the relevant disease by therapeutic targeting of newly discovered mechanisms causing skeletal muscle atrophy, lire present invention also proposes methods for developing, preparing, and applying pharmaceutical formulations comprising the relevant inhibitors.

The present invention provides a multiomics approach, which integrate single-cell RNA-sequencing (scRNA-seq) and spatiotemporal transcriptomics (ST) offering potential for dissecting transcriptional networks and revealing cell-cell interactions involved in biomolecular pathomechanisms. The present invention also provides a multimodal approach combining high-throughput scRNA-seq and ST to elucidate XLRS-specific transcriptomic signatures in two XLRS-like models with retinal splitting phenotypes, including genetically engineered (Rs1emR209C) mice and patient-derived retinal organoids harboring the same patient-specific p.R209C mutation. Through multiomics transcriptomic analysis, the endoplasmic reticulum (ER) stress / eIF2 signaling, mTOR pathway, and the regulation of eIF4 and p70S6K pathways as chronically enriched and highly conserved disease pathways between two XLRS-like models are identified. Western blots and proteomics analysis validated the occurrence of unfolded protein responses, chronic eIF2α signaling activation, and chronic ER stress-induced apoptosis. Furthermore, therapeutic targeting of the chronic ER stress / eIF2α pathway activation synergistically enhanced the efficacy of AAV mediated RS1 gene delivery, ultimately improving bipolar cell integrity, postsynaptic transmission, disorganized retinal architecture and electrophysiological responses. Collectively, the complex transcriptomic signatures obtained from Rs1emR209C mice and patient-derived retinal organoids using the multiomics approach provide opportunities to unravel potential therapeutic targets for incurable retinal diseases, such as XLRS.

According to the immune checkpoint molecule and the pharmaceutical application thereof, a kit for detecting ILDR2 comprises an antibody specifically combined with ILDR2 protein or a primer pair for detecting ILDR2 mRNA, and the kit is used for detecting the expression level of ILDR2 in a liver cancer tissue sample in vitro. The invention discloses application of detection of B7 family protein ILDR2 expression quantity in liver cancer diagnosis and treatment. It is found for the first time that ILDR2 is highly expressed in liver cancer, and the highly expressed ILDR2 is poorly related to prognosis of patients. Liver cancer cells express ILDR2 to inhibit the anti-tumor function of CD4 + T cells, promote formation of regulatory T cells and inhibit polarization of the CD4 + T cells to Th1. The ILDR2 is knocked down, so that liver cancer cell proliferation can be obviously inhibited. Detection of ILDR2 expression can better guide treatment of liver cancer patients with high ILDR2 expression, and targeted ILDR2 can screen candidate immune checkpoint drugs for treating liver cancer.

The invention discloses a xanthohumol lung cancer targeted therapy method based on an exosome delivery system and application of the xanthohumol lung cancer targeted therapy method, and relates to the technical field of biological medicine and drug targeted delivery, in particular to the xanthohumol lung cancer targeted therapy method based on the exosome delivery system and the application of the xanthohumol lung cancer targeted therapy method. The lemon-derived exosome is used as a carrier, so that the enrichment effect of xanthohumol in tumor tissues is effectively improved, and the anti-tumor effect of xanthohumol is enhanced; the xanthohumol regulates a lung cancer immune microenvironment by influencing an immune checkpoint PD-L1; wherein the immunomodulatory effect is optimized, the treatment effect is improved, and tumor-related immunosuppression is relieved; in order to solve the problem that the effect of a traditional xanthohumol delivery mode is limited, an exosome delivery platform is adopted, and the delivery efficiency and the treatment targeting property of the medicine are further improved by utilizing the natural targeting property and the low immunogenicity of the exosome delivery platform; through an intelligent delivery system, the toxicity of xanthohumol to normal tissues is reduced.

The present disclosure provides methods of identifying a subject with cancer that is non-responsive a treatment (e.g., immune checkpoint inhibitor monotherapy), wherein the cancer has an altered (e.g., increased or decreased) expression level of a panel of biomarkers, and methods of using the same to provide a combination therapy (e.g., a therapeutic targeting myeloid immune suppressive checkpoint (e.g., LAIR1) and an immune checkpoint inhibitor) to the subject with cancer.

The application relates to the technical field of tumor drugs, in particular to application of METTL5 as a tumor immunotherapy targeting site. The base sequence of the METTL5 is shown in SEQ ID No. 1; wherein the METTL5 is a brand-new RNAm6A methyltransferase, is closely related to ribosome translation function, and can regulate the translation of a tumor immune key regulator IL-27; therefore, the METTL5 is used as the tumor immunotherapy targeting site, the expression of the METTL5 related genes or coding proteins is inhibited through targeting, the body anti-tumor immunity can be effectively stimulated, the METTL5 becomes the targeting site capable of enhancing the response rate of tumor immunotherapy, and the METTL5 used as the tumor treatment target point has a wide application prospect in the anti-tumor immunotherapy.

To provide a specific therapeutic targeting system based on the control of microglial cell activation.SOLUTION: Provided is a method of decreasing microglial activation comprising contacting a microglial cell with an anti-CD3 antibody.SELECTED DRAWING: None

The subject matter disclosed herein is generally directed to treating cancers sensitive to phosphate dysregulation with inhibitors of inositol pyrophosphate (PP-InsP) synthesis, in particular, inhibitors of inositol hexakisphosphate kinases IP6Ks.

The invention discloses a miRNA molecular sponge and application thereof in preparation of drugs for treatment or adjuvant treatment of brain glioma, PLK1 gene is taken as a treatment target gene, mir-1301-3p is taken as a target spot, the miRNA molecular sponge absorbs mir-1301-3p to block interaction between the mir-1301-3p and mRNA of the PLK1 gene so as to down-regulate PLK1 protein expression, and the miRNA molecular sponge can be used for treating brain glioma. Therefore, the effect of treating or adjunctively treating brain glioma is achieved. Bioinformatics analysis and experimental verification show that hsa-mir-1301-3p can be specifically combined with a 3UTR (Untranslated Region) region of a PLK1 gene, and is different from the down-regulation effect of conventional microRNA (Ribonucleic Acid) on the expression of a target gene protein, and the has-mir-1301-3p has a promotion effect on the expression of the PLK1 gene; according to the present invention, the combination of has-mir-1301-3p and the 3UTR region of the mRNA of the PLK1 gene is blocked by using the microRNA sponge technology, such that the expression of the PLK1 protein can be down-regulated, and the growth amplification of the brain glioma cells, the formation of the adherent form and the drug resistance are inhibited so as to achieve the treatment effect. The invention provides a new thought and method for the treatment of brain glioma.

The invention relates to a copolymer with tissue adhesion and ROS (reactive oxygen species) response performance, a drug-loaded nanoparticle as well as a preparation method and application of the copolymer and the drug-loaded nanoparticle. The copolymer is formed by copolymerizing a diacrylate compound and an amino-containing compound, the diacrylate compound is selected from one or more of compounds as shown in a formula (I); the amino-containing compound is selected from one or more of compounds as shown in a formula (II-1) and a formula (II-2) or salts or stereoisomers thereof. The copolymer can deliver a drug for treating gastrointestinal oxidative stress related diseases to a diseased region in a targeted manner, can release a therapeutic drug in a responsive manner at the diseased region, has good gastric mucosa adhesion capability, and can improve local drug concentration, so that the therapeutic targeting and curative effect persistence of the drug are enhanced, and the curative effect of the drug is improved. The treatment effect is enhanced. # imgabs0 #

Populations of CAR T cells that exhibit reduced trogocytosis are disclosed, as well as methods for making such cells and methods of using such cells in the treatment of cancer. A reduction in trogocytosis is achieved by inhibiting Cathepsin B in the CAR T cells and / or inducing ubiquitylation of cancer antigens taken up by the CAR T cells.

Disclosed are methods of treatment and inhibitors for gastrointestinal stromal tumor (GIST) in a subject, with an active agent that inhibits a Menin or a member of the Menin-MLL complex.

The invention discloses a small molecule lysosome targeting chimera and application thereof, and relates to the technical field of medicines. The invention relates to a small molecule lysosome targeting chimera (eHSPTACs). The structural formula of the small molecule lysosome targeting chimera (eHSPTACs) is as follows: L1-Linker-L2, wherein, L1 is an HSP90 ligand; l2 is a target protein ligand; and the Linker is a connexon. The invention develops an eHSP90 mediated micromolecule lysosome targeting chimera, and lysosome pathway degradation of secreted protein and membrane protein can be effectively realized by coupling an HSP90 ligand and a secreted protein / membrane protein ligand; the technology can be used for treating related diseases of targeted secretory protein and membrane protein, such as tumors, immunity, inflammation and the like.

In various embodiments human anti-CD46 antibodies that are internalizing and enter tumor cells via the macropinocytosis pathway are provided, as well as antibody-drug conjugates (ADCs) developed from these antibodies for diagnostic and / or therapeutic targeting of CD46-overexpressing tumors.

A method of using an EDA2R inhibitor or an NIK inhibitor and an OSMR inhibitor for the treatment and / or prevention of the relevant disease is provided, where the treatment and / or prevention is performed by therapeutic targeting of newly discovered mechanisms causing skeletal muscle atrophy. The present invention also proposes methods for developing, preparing, and applying pharmaceutical formulations including the relevant inhibitors.

The present invention relates to a biomarker composition for diagnosing resistance to BCR-ABL-independent tyrosine kinase inhibitors (TKIs), including FAM167A, and a composition for preventing or treating chronic myeloid leukemia that targets FAM167A. More specifically, the present invention provides a composition, kit, and method for diagnosing BCR-ABL-independent TKI resistance in chronic myeloid leukemia patients by confirming the mRNA expression level of the FAM167A protein, a fragment thereof, or a gene encoding the protein, as well as a pharmaceutical composition for preventing or treating chronic myeloid leukemia exhibiting BCR-ABL-independent TKI resistance that targets FAM167A, and a pharmaceutical composition for inhibiting BCR-ABL-independent TKI resistance in chronic myeloid leukemia patients.

The present application relates to macropinocytic human anti-CD46 antibodies and targeted cancer therapies. In various embodiments, human anti-CD46 antibodies that are internalized via the macropinocytic pathway and enter tumor cells, as well as antibody-drug conjugates ADCs developed from these antibodies for diagnostic and / or therapeutic targeting of CD46 overexpressing tumors are provided.

The invention provides a BRCA specific siRNA which is used for enhancing the sensitivity of cancer cells to a PARP inhibitor. According to the present invention, the siRNA can be combined with the PARP inhibitor to induce cancer cell death, and is suitable for patients having the wild-type BRCA gene and having the low treatment effect on the PARP inhibitor. According to the present invention, the fusion protein-siRNA complex for delivering the siRNA can be absorbed by cells through CD47 mediation, such that the fusion protein-siRNA complex can be specifically delivered to cancer cells, and can be efficiently absorbed by the cells so as to maximize the desired cell death effect.

The invention belongs to the technical field of biological medicines, and particularly relates to application of DNA / RNA heterodouble-stranded oligonucleotide of SYK in preparation of a medicine for inhibiting intrahepatic cholangiocarcinoma (ICC) metastasis. The DNA / RNA heteroduplex oligonucleotide (SYK-HDO) of SYK disclosed by the invention is combined with a low-density lipoprotein receptor (LDLR) through cholesterol modification, so that ICC cells with high LDLR expression are specifically targeted, and the treatment targeting is improved; sYK-HDO is actively delivered to tumor cells by utilizing LDLR-mediated endocytosis, so that the local drug concentration is improved, and the drug administration frequency is reduced; in addition, due to the DNA-RNA double-strand structure of the polypeptide, the polypeptide is not easy to degrade by nuclease in blood circulation; and finally, the SYK-HDO can stably silence the expression of the SYK gene of the bile duct cancer cell line through a gene silencing mechanism, so that the possible off-target effect and drug resistance of the SYK kinase inhibitor can be avoided.

This invention relates to a method for preparing drug-loaded nanoparticles that regulate the tumor microenvironment. The steps include: S1, dispersing CaCO3 nanoparticles in a first solvent, adding dopamine hydrochloride solution, lysine solution, and ammonia, reacting for a first time, terminating the reaction, and separating the solid and liquid to obtain the first nanoparticles; S2, dispersing the first nanoparticles in a second solvent, adding alendronate sodium solution, adjusting the pH to neutral, reacting for a second time to obtain the second nanoparticles; S3, dispersing the second nanoparticles in a second solvent, adding dimethyl sulfoxide, shikonin solution, and dihydroporphyrin E6 solution, reacting for a third time, and separating the solid and liquid to obtain the drug-loaded nanoparticles. The drug-loaded nanoparticles of this invention can be used for multi-target therapy, targeting tumor cells. In addition to directly killing tumor cells with ROS generated by PDT and SHK, they induce ICD in cancer cells, reverse the acidic tumor microenvironment, and increase CD4+. + T cell infiltration and a reduction in Treg cells.

The invention provides a renal cell carcinoma prognosis lifetime prediction method based on internal and external verification of a data set, and relates to the field of clinical medical diagnostics. The clinical factors related to the prognosis lifetime of the renal cell carcinoma, such as complications, tumor size, lymph node metastasis, tumor remote metastasis, tumor grading, tissue types, immunotherapy and targeted therapy, can efficiently predict the prognosis survival probability of a renal cell carcinoma patient, and can improve the identification accuracy of a prediction model; therefore, reference is provided for treatment of renal cell carcinoma patients.

A method of detecting triple negative breast cancer (TNBC) is provided. Overexpression of ICAM-1 is linked to an increased risk of TNBC. A composition of matter is also provided that binds an anti-ICAM˜1 antibody to a nanoparticle. The composition may be used as an imaging agent and / or a therapeutic targeting agent. A therapeutically active molecule may be bound to the composition to provide targeted therapy.

The application discloses a nano-focal anaphylaxis drug targeting CD47 protein and preparation and application thereof, and belongs to the technical field of drugs. The nano-focal anaphylaxis drug is a micellar nanoparticle formed by self-assembly of an amphiphilic carrier material and a focal anaphylaxis prodrug, the amphiphilic carrier material is composed of an amphiphilic polymer with a hydrophilic end modified with a CD47 targeting peptide and an amphiphilic polymer without modification, and the focal anaphylaxis prodrug is a prodrug formed by reduction response chemical bond connection of lonidamide or 3-bromopyruvic acid. The nano-focal anaphylaxis drug provided by the application can realize precise tumor treatment, the CD47 targeting peptide realizes efficient targeted delivery and accumulation of the drug in the tumor, the release of the focal anaphylaxis prodrug is triggered by higher reduction medium level in tumor tissues, and tumor cells are induced to undergo focal anaphylaxis. In normal tissues, the nano drug cannot induce normal cell focal anaphylaxis, and therefore the tumor selectivity of the nano drug is significantly enhanced.

The present invention relates to isolated antibodies, fragments thereof and antibody-drug conjugates that bind to Lymphocyte antigen 6 family member K (LY6K) and their use for screening for LY6K-positive malignant cells or for therapeutic targeting of LY6K-positive malignant cells.