175 results about "Cadherin" patented technology

The invention relates to a nano antibody targeting cadherin 17 and application thereof, and relates to the technical field of immunology and molecular biology, the amino acid sequence of a complementary determining region of the nano antibody targeting cadherin 17 comprises CDR1 shown as any one of SEQ ID NO: 21-32, CDR2 shown as any one of SEQ ID NO: 34-45, and CDR3 shown as any one of SEQ ID NO: 47-58. According to the invention, an alpaca immune phage display library is constructed, a series of nano antibody molecules targeting cadherin 17 (CDH17) are screened from the alpaca immune phage display library, and functions and applications of the nano antibody are verified at various levels of CDH17 antigen protein, CDH17 target cells, CDH17 CAR-T cells and the like.

The invention relates to a humanized nano antibody targeting cadherin 17 and application of the humanized nano antibody, and relates to the technical field of immunology and molecular biology. The complementarity determining region of the humanized nano antibody comprises a CDR1 of which the amino acid sequence is shown as SEQ ID NO: 2, a CDR2 of which the amino acid sequence is shown as SEQ ID NO: 4 and a CDR3 of which the amino acid sequence is shown as SEQ ID NO: 6; a framework region of the humanized nano antibody comprises an FR1 of which the amino acid sequence is shown as any one of SEQ ID NO: 1 and SEQ ID NO: 8, an FR2 of which the amino acid sequence is shown as any one of SEQ ID NO: 3, SEQ ID NO: 9 and SEQ ID NO: 11, an FR3 of which the amino acid sequence is shown as any one of SEQ ID NO: 5 and SEQ ID NO: 10, and an FR4 of which the amino acid sequence is shown as SEQ ID NO: 7. According to the humanized nano-antibody, the immunogenicity of the nano-antibody is reduced, the targeted binding activity and killing activity are improved, and the humanized nano-antibody can be used for developing immunodetection reagents, CAR-T / NK cell drugs and antibody drugs.

The invention relates to a detection kit for epithelial-mesenchymal transition in EB virus infected thymoma and application, the detection kit comprises a quantum dot labeled antibody E-Cadherin and a quantum dot labeled antibody Vimentin, a quantum dot is coupled with a specific antibody, a thymoma paraffin section sample is dyed through the quantum dot and the specific antibody conjugate, and the EB virus infected thymoma is obtained. The conjugate can be specifically connected with an EMT related antigen expressed in the slice, so that the quantum dots can be used for qualitative or quantitative detection of the EMT-generated thymoma cells. The quantum dots are used for replacing fluorescent dye, direct marking of tissue slices can be achieved, local positioning of epithelial cells and mesenchymal tissues in the thymoma microenvironment is achieved, number detection and position detection can be achieved, and EMT condition evaluation is facilitated.

To provide an antitumor drug having an excellent therapeutic effect, which is excellent in terms of antitumor effect and safety. Provided is an anti-cadherin 17 antibody comprising a heavy chain variable region and a light chain variable region, a drug conjugate thereof, and a composition containing the anti-cadherin 17 antibody or the drug conjugate thereof, and an application thereof as a drug.

The invention provides an antibody specifically combined with CDH6 (cadherin 6) and application thereof, and particularly discloses mouse and humanized antibodies combined with CDH6 as well as a preparation method and application thereof, and the mouse and humanized antibodies have better affinity with CDH6 protein and better endocytosis activity, so that the mouse and humanized antibodies can be applied to preparation of medicines for treating tumors and the like.

Provided are antibodies or antigen-binding fragment thereof having binding specificity to the human cadherin 17 (CDH17) protein and antibody-drug conjugates (ADC) thereof. These antibodies and ADCs are capable ofbinding to CDH17 with high selectivity, bystander effect and anti-tumor effect. Also provided are methods and uses for treating cancers.

The invention discloses an effectiveness exploration method for inhibiting AM by exciting LIPUS through a flexible ultrasonic patch, and belongs to the field of medical equipment and biomedical engineering. The patch comprises a flexible substrate, an island bridge type metal electrode, an adjustable array type piezoelectric ceramic unit and a flexible packaging layer, can be precisely attached to a focus area, outputs low-intensity pulse ultrasound with the frequency of 1-3 MHz and the sound intensity of 30-120 mW / cm < 2 >, and can inhibit expression of proinflammatory factors, up-regulate E-cadherin, induce apoptosis of ectopic endometrial cells and inhibit activity of pain ion channels, so that the pain of a patient is relieved, and the pain of the patient is relieved. In-vivo and in-vitro experiments show that the patch does not have significant uterus and ovarian toxicity, can reduce the fibrosis area by 40% or more, can increase the apoptosis rate to 45%, supports a continuous or pulse type adjustable treatment mode, integrates a flexible electronic technology and ultrasonic medicine, and has a wide application prospect. A noninvasive, accurate and wearable innovative treatment scheme is provided for adenomyosis, and the clinical transformation value is remarkable.

The invention provides application of G3BP1 in preparation of a medicine for protecting barrier function integrity of vascular endothelial cells, and belongs to the technical field of biological medicine manufacturing. The invention provides application of G3BP1 in preparation of a medicine for protecting barrier function integrity of vascular endothelial cells. The present invention relates to G3BP1 that ensures the sustained expression of key adherent junction proteins (VE-cadherin, p120) by directly binding to and stabilizing the mRNA of these proteins; meanwhile, the G3BP1 is combined with the MYD88mRNA to promote the degradation of the MYD88mRNA, so that a permeability-promoting MYD88-ARNO-ARF6 signal channel is inhibited, especially under the condition of an inflammation period. Therefore, the G3BP1 regulates and maintains the integrity of the vascular barrier through double transcription, and a new treatment strategy is provided for damage repair of the functional integrity of the vascular endothelial cell barrier.

The invention belongs to the technical field of biology, and particularly relates to an endogenous cell aggregate source exosome and application thereof.The exosome is obtained by culturing mesenchymal stem cells in a 3D cell culture system added with a cell culture medium and IGF-1 to obtain mesenchymal stem cell aggregates and secreting the mesenchymal stem cell aggregates in a culture medium; the cell culture medium is prepared from the following components in parts by weight: 1 to 3 parts of hE-cad-Fc and 1 to 3 parts of hN-cad-Fc. The preparation method of the mesenchymal stem cell source exosome pretreated by combining the cadherin with the IGF-1 has extremely high exosome production efficiency, and the prepared mesenchymal stem cell source exosome pretreated by combining the cadherin with the IGF-1 is complete in structure, uniform in particle size distribution, high in production efficiency and high in effective functional component content.

The invention provides an anti-CDH17 antibody or an antigen binding fragment thereof, a CDH17-targeted antibody drug conjugate (ADC) and application thereof. The anti-CDH17 antibody provided by the invention can be specifically combined with CDH17 protein, and has a relatively strong CDH17 expression tumor cell killing effect, so that the anti-CDH17 antibody has high-specificity treatment application potential of CDH17 expression tumor. Furthermore, the anti-CDH17 antibody provided by the invention can be effectively internalized on CDH17 expression tumor cells, ADC formed by coupling the anti-CDH17 antibody with a small-molecule toxic compound keeps high internalization activity and strong binding capacity to target protein CDH17, and shows high killing activity to the CDH17 expression tumor cells.

The present application provides antigen-binding proteins (e.g., antibodies such as single-domain antibodies) that specifically bind cadherin 17 (CDH17). The application also provides fusion proteins and conjugates comprising the antigen-binding proteins, polynucleotides and recombinant vectors encoding the antigen-binding proteins, as well as host cells and methods for preparing the antigen-binding proteins. The application further provides pharmaceutical compositions comprising the antigen-binding proteins and methods for treating a disease or disorder using the antigen-binding proteins.

The invention relates to the technical field of biology, in particular to a matrix-enabled mesenchymal stem cell aggregate and application, and the matrix-enabled mesenchymal stem cell aggregate is obtained by subculturing matrix-enabled mesenchymal stem cells in a 3D cell culture system. The matrix-enabled mesenchymal stem cells are obtained by subculture of mesenchymal stem cells in a cell culture matrix, and the cell culture matrix is prepared from 1-3 parts of hE-cad-Fc and 1-3 parts of hN-cad-Fc. Endogenous epithelium cadherin and nerve cadherin are highly expressed in cell aggregation cells, so that transcription factors are promoted to enter nuclei, the expression levels of anti-inflammatory immune regulation related factors and matrix degradation and cell migration related factors are up-regulated, and activated macrophages are promoted to be polarized to M2 type macrophages; the effects of anti-inflammation, immune regulation, tissue damage repair and the like of intravenous implantation of the matrix-enabled mesenchymal stem cell aggregate for treating diseases such as hepatic fibrosis, diabetes mellitus, nerve injury and the like are remarkably improved.

The invention discloses application of 2-aminoethoxy diphenyl borate (2-APB) in preparation of a medicine for improving endometrial receptivity and treating diseases related to the endometrial receptivity, and belongs to the technical field of biological medicine. A large number of experiments prove that 2-APB specifically activates a TRPM6 channel, enhances calcium ion influx and activates a calcium-dependent CaM-CaMKII-Ecadherin signal axis, so that expression of receptivity markers (such as E-cadherin and ICAM-1) is up-regulated, and endometrial receptivity is improved. The problems of poor targeting property and high toxicity of the traditional calcium ion carrier are solved, and a safe and effective treatment strategy is provided for a patient suffering from repeated implantation failure (RIF).

The present invention relates to anti-CD 103 antibodies, as well as use of these antibodies in diagnosis, prognosis, monitoring, and treatment of diseases. Also disclosed is an imaging agent comprising the anti-CD 103 antibody and a detectable label, wherein the antibody either does not block CD 103 binding to E-cadherin or at least partially blocks CD 103 binding to E-cadherin. The methods of treatment involve administering the anti CD 103 antibody which may be optionally coupled to a cytotoxic agent. Diseases to be treated include e.g. Hairy Cell leukemia, HCLv, intestinal and extraintestinal lymphomas, enteropathy-associated T-cell lymphoma (EATL), T-lymphoblastic leukemia / lymphoma (T-ALL), T-cell prolymphocytic leukemia (T-PLL), adult T cell leukemia / lymphoma (ATLL), mycosis fungoides (ME), anaplastic large cell lymphoma ALCL, cutaneous T-cell lymphoma (CTCL), Sezary Syndrome (SS), Alzheimer's disease, Parkinson's disease or multiple sclerosis.

The present invention provides a kind of radix schizonepetae extract for treating ulcerative colitis and its preparation method and application, and relates to the field of biomedicine technology. The preparation method of the radix schizonepetae extract of the present invention comprises: soaking radix schizonepetae in water, heating and boiling, condensing and refluxing, filtering, and collecting the filtrate, which is the radix schizonepetae extract. The radix schizonepetae extract of the present invention can reduce collagen deposition and intestinal epithelial cell apoptosis in the colon epithelium of ulcerative colitis, has the effect of downregulating the abnormally high expression of genes and proteins such as N-cadherin, IntegrinA1, Vinculin, TGF-β2, Srcin, etc. in the colon tissue of ulcerative colitis, reduces colon fibrosis and inflammatory damage, protects the barrier function of the colon epithelium, and has the effect of inhibiting the overexpression of Wnt 5A / B and β-Catenin proteins caused by DSS, and alleviates colon fibrosis, thereby achieving the effect of treating ulcerative colitis and alleviating colon fibrosis.

The present application is related to a panel of antibody-drug conjugates (ADCs) in which cytotoxic tubulin inhibitor monomethyl auristatin E (MMAE) is conjugated onto monoclonal antibodies targeting cadherin-17 (CDH17), a tumor-associated antigen that is overexpressed in uterine cervical adenocarcinoma, mucinous carcinoma of the ovary, and gastrointestinal cancers including pancreatic, gastric, colorectal cancers, etc. These ADCs recognise different parts of CDH17, showing high-affinity binding to CDH17-expressing cells. All these properties allow the CDH17-targeting ADCs to demonstrate cytotoxicity specifically against CDH17-expressing cancer cells. The cytotoxic effect of MMAE would be highly localized in tumors, maximising the anti-tumor effect and simultaneously reducing the adverse effects of anti-cancer drug on non- cancerous normal tissues.

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.

The present invention discloses a calcium carbonate-conjugated polymer composite nanoparticle with anti-tumor and anti-metastasis effects and its application. The nanoparticles rupture and decompose in the weakly acidic microenvironment of the tumor, releasing the conjugated polymer and a large amount of Ca 2+ The conjugated polymer can generate reactive oxygen species or heat energy to kill tumor cells under light. In addition, reactive oxygen species can also put tumor cells in a state of high oxidative stress, causing mitochondrial dysfunction and desensitization of calcium ion-related channels, causing intracellular "calcium overload" and inducing tumor cell death. These multiple effects make the nanoparticles highly effective in cancer treatment. Extracellular Ca 2+ Increased levels can enhance the adhesion between tumor cells by regulating the morphology of cadherin, thereby inhibiting tumor cell migration. In this invention, the calcium carbonate-conjugated polymer composite nanoparticles have excellent anti-tumor and anti-metastasis effects, providing a new approach for the comprehensive treatment of cancer.

The present invention is related to a P-cadherin binding compound; a composition comprising the P-cadherin binding compound; the P-cadherin binding compound and the composition, respectively, for use in a method for the diagnosis of a disease; the P-cadherin binding compound and the composition, respectively, for use in a method for the treatment of a disease; the P-cadherin binding compound and the composition, respectively, for use in a method of diagnosis and treatment of a disease which is also referred to as "thera(g)nosis" or "thera(g)nostics"; the P-cadherin binding compound and the composition, respectively, for use in a method for delivering a radionuclide to a P-cadherin expressing tissue; a method for the diagnosis of a disease using the P-cadherin binding compound and the composition, respectively; a method for the treatment of a disease using the P-cadherin binding compound and the composition, respectively; a method for the diagnosis and treatment of a disease which is also referred to as "thera(g)nosis" or "thera(g)nostics, using the P-cadherin binding compound and the composition, respectively; a method for the delivery of a radionuclide to a P-cadherin expressing tissue using the P-cadherin binding compound and the composition, respectively.

The invention provides a method for promoting differentiation of induced pluripotent stem cells to trigerm layers and application of the method in differentiation potential detection, and relates to the technical field of biologication.The method comprises the steps that the induced pluripotent stem cells are inoculated into a culture medium containing 5-20 [mu] M of E-cadherin activator 1, shaking culture is conducted to form embryoid bodies, the embryoid bodies are added into a differentiation culture medium for differentiation culture, and the embryoid bodies are obtained. Obtaining an embryoid body for activating three-germ-layer differentiation potential; inoculating the embryoid body which activates the differentiation potential of the three-germ layer into a container coated with a cell adhesion matrix, adding a differentiation culture medium, continuing differentiation culture, and performing induced differentiation to form the three-germ layer cells. The technical problems that in the prior art, when iPSC is induced to be differentiated to three germ layers through an embryoid body path, the embryoid body forming capacity is poor, the embryoid body state is poor, the long-term maintaining capacity is poor, and the endoderm differentiation and climbing-out capacity is poor due to the fact that the embryoid body is poor in wall attaching capacity after plate rotation are solved.

The invention relates to the technical field of biomedicine detection, and discloses a tumor cell marker detection system for predicting the activation state of intracellular protein kinase. Comprising a marker detection module used for qualitatively detecting epithelial cell markers, mesenchymal cell markers, cell polarity markers and extracellular matrix related markers in tumor cells; the data processing module is used for performing cross validation on an epithelial cell marker, a mesenchymal cell marker, a cell polarity marker and an extracellular matrix related marker; the dynamic weighting module is used for performing dynamic weighting on different markers based on a complex system theory, and endowing epithelial cadherin with a higher weight; and the judgment module is used for determining whether epithelial intercellular substance transformation occurs or not according to the dynamically weighted marker data, and predicting the activation state of intracellular phosphoinositide 3-kinase alpha and the invasiveness of tumor cells based on the determination result of the epithelial intercellular substance transformation.

The present invention aims to provide a marker for diagnosing non-alcoholic fatty liver disease (NAFLD). The above-mentioned problem has been solved by a marker for diagnosing non-alcoholic fatty liver disease (NAFLD), said marker being at least one protein selected from the group consisting of endopeptidases, hydrolases, calcium ion-binding proteins, cytoskeletal proteins, transferases, receptor-binding proteins, phosphatases, antigen-binding proteins, RNA-binding proteins, reductases, and cadherin-binding proteins, or a gene encoding said protein.

The present invention discloses the preparation of patchouli flavonoid nanoliposomes and their application in inhalation treatment of acute lung injury, and relates to the field of medical technology. The patchouli flavonoid nanoliposomes provided by the present invention prepare patchouli flavonoids into a liposome dosage form, which has good stability and biocompatibility. The drug is administered to mice with acute lung injury, so that patchouli flavonoids can act on the mouse lungs in a targeted manner, reduce the expression of inflammatory factors such as IL-6, IL-1β and TNF-α in the mouse lungs to relieve inflammation, improve pulmonary edema, and reduce lung tissue damage, while increasing the levels of tight junction factors such as ZO-1, VE-Cadherin, E-Cadherin and Claudin5 to repair lung barrier damage. The present invention is expected to provide an effective strategy for the treatment of acute lung injury.

Peptides for use in systems that prevent the interaction of the FadA protein released from the Fusobacterium nucleatum (F. nucleatum) bacterium with E-cadherin, which has a carcinogenic effect, or the inhibition of the microorganism with antimicrobial agents and that will inhibit the carcinogenesis mechanisms of F. nucleatum infection and enable the development of therapeutic systems against infections that may occur due to the decreased immunity of patients undergoing cancer treatment with the use of peptides with anti-cancer and antimicrobial properties by developing ten peptides with FadA protein binding energy greater than −11.6 kcal / mol. Peptides with anticancer and antimicrobial properties allow the development of therapeutic systems to prevent F. nucleatum infection, to prevent cancer development after F. nucleatum infection, or to develop therapeutic systems against infections that occur due to the decreased immunity of cancer patients due to cancer treatment.

The invention discloses application of a lactic acid modified gene ENO1 inhibitor in preparation of a medicine for treating nasopharynx cancer, and relates to the technical field of biological medicines. A head and neck squamous cell carcinoma prognosis model containing seven lactylation related genes is constructed by analyzing a TCGA database, the model can effectively distinguish patient risks, the total lifetime of a high-risk group is remarkably shortened, and a risk score is an independent prognosis factor; the functions of the key gene ENO1 are deeply studied through in-vitro experiments, and experimental results show that silencing of the ENO1 gene in nasopharynx cancer 5-8F cells causes up-regulation of cell pan-lactylation level, up-regulation of MMP2 expression and down-regulation of E-cadherin expression, and migration and invasion ability of tumor cells is significantly enhanced. The prognosis model provided by the invention has an important clinical prediction value, inhibition of ENO1 can promote tumor progression through abnormal lactylation, and a new thought is provided for taking ENO1 as a treatment target.

The invention provides modRNA (Ribonucleic Acid) for treating obliterated bronchitis, and belongs to the technical field of bioengineering. The modRNA for treating obliterated bronchitis provided by the invention is composed of an IL-10 modRNA (Interleukin-10) and an IFN (Interferon)-alpha modRNA (Interferon-alpha) modRNA. The BO treatment effect is achieved by inhibiting bronchial epithelial cell epithelial-mesenchymal transition (EMT), the expression of alpha-SMA and Vimentin in lung tissue can be remarkably reduced, the expression of E-cadherin and Cytokeratin 5 can be up-regulated, microbronchial epithelial injury is repaired, collagen deposition is reduced, and the lung function is improved. The synergistic effect of the two is better than that of single gene therapy, the safety is high, and the controllability is strong.

The present invention relates to humanized nanobodies targeting cadherin 17 and their applications, and to the technical fields of immunology and molecular biology. The complementary determining region of the humanized nanobody includes a CDR1 with an amino acid sequence as shown in SEQ ID NO: 2, a CDR2 with an amino acid sequence as shown in SEQ ID NO: 4, and a CDR3 with an amino acid sequence as shown in SEQ ID NO: 6; the framework region of the humanized nanobody includes a FR1 with an amino acid sequence as shown in any one of SEQ ID NO: 1 and SEQ ID NO: 8, an FR2 with an amino acid sequence as shown in any one of SEQ ID NO: 3, SEQ ID NO: 9, and SEQ ID NO: 11, an FR3 with an amino acid sequence as shown in any one of SEQ ID NO: 5 and SEQ ID NO: 10, and an FR4 with an amino acid sequence as shown in SEQ ID NO: 7. The humanized nanobody of the present invention reduces the immunogenicity of the nanobody, improves the target binding activity and killing activity, and can be used to develop immune detection reagents, CAR-T / NK cell drugs, and antibody drugs.

Described herein is an antigen binding polypeptide that specifically binds cadherin 17 (CDH17). Also described herein is a chimeric antigen receptor (CAR) comprising the antigen binding polypeptide as the antigen binding domain, a CAR-T cell expressing the CAR, as well as a method of treating diseases or disorders caused by or involving CDH17-positive cells, such as CDH17-positive cancers, using the antigen binding polypeptide or the CAR-T cell.

An aptamer composition is disclosed which has one or more oligonucleotides that include at least one of deoxyribonucleotides, ribonucleotides, derivatives of deoxyribonucleotides, derivatives of ribonucleotides, or mixtures thereof. The aptamer composition has a binding affinity for one or more cellular membrane glycoproteins selected from the group consisting of: intercellular adhesion molecule 1 (ICAM-1), low-density lipoprotein receptor (LDLR) family members, and cadherin-related family member 3 (CDHR3), preferably intercellular adhesion molecule 1 (ICAM-1), and is configured to reduce the binding of one or more human rhinoviruses to the intercellular adhesion molecule 1 (ICAM-1).

The invention discloses an application of glabridin in preparation of related drugs for inhibiting epithelial-mesenchymal transition in inflammatory bowel diseases. In the epithelial-mesenchymal transformation process, epithelial cells lose cell polarity and intercellular connection, are transformed into mesenchymal cells in function and morphology, directly participate in fibroblast activation and extracellular matrix deposition and cause intestinal fibrosis, and are one of anti-fibrosis targets. According to the application of the glabrione in preparation of the medicine related to inhibition of epithelial-mesenchymal transition in the inflammatory bowel disease, provided by the invention, the expression change of epithelial cell markers Claudin-1 and E-cadherin caused by TGF-beta 1 and interstitial cell markers Vimentin, N-cadherin, Snail and alpha-SMA can be relieved, cell migration caused by TGF-beta is improved, and the epithelial-mesenchymal transition induced by TGF-beta 1 is inhibited. The research on the mechanism of action shows that by blocking a TGF-beta1 / Smad2 / 3 signal channel and inhibiting AKT1 activation and inhibition of epithelial-mesenchymal transition, the application of the compound in inhibition of epithelial-mesenchymal transition and prevention of intestinal disease related fibrosis is prompted.