17 results about "Binding inhibition" patented technology

Provided are an anti-ST2 antibody and a pharmaceutical composition. Specifically provided is an anti-ST2 antibody or an antigen-binding fragment thereof. The anti-ST2 antibody comprises a heavy chain variable region and a light chain variable region. The heavy chain variable region comprises HCDR1 to HCDR3, and the light chain variable region comprises LCDR1 to LCDR3, wherein the amino acid sequence of HCDR1 is as shown in SEQ ID NO: 1, the amino acid sequence of HCDR2 is as shown in SEQ ID NO: 2, and the amino acid sequence of HCDR3 is as shown in SEQ ID NO: 3; and the amino acid sequence of LCDR1 is as shown in SEQ ID NO: 4, the amino acid sequence of LCDR2 is as shown in SEQ ID NO: 5, and the amino acid sequence of LCDR3 is as shown in SEQ ID NO: 6. The antibody can bind to human ST2, block the binding of human IL-33 to ST2, and inhibit the activation of downstream signaling pathways of a human IL-33 / ST2 pathway.

This invention discloses an HBB-derived peptide and its use in the preparation of drugs for treating tumors. The HBB-derived peptide comprises a combination peptide consisting of a polypeptide with amino acids 30-40 at the N-terminus of HBB (as shown in SEQ ID NO:2) linked to a transmembrane peptide TAT (as shown in SEQ ID NO:3). The combination peptide is formed by modifying its N-terminus or C-terminus, through amino acid deletion, substitution, cyclization, or chiral conversion. Specifically, the amino acid sequence of this HBB-derived peptide, as shown in SEQ ID NO:1, is composed of a polypeptide with amino acids 30-40 at the N-terminus of HBB linked to a transmembrane peptide TAT. It can specifically block the binding of HBB to NDUFAF5, inhibit the proliferation of chemotherapy-resistant lung cancer cells and tumor growth, and reverse chemotherapy resistance, thus possessing significant clinical application value.

This invention belongs to the field of biomedicine and relates to an anti-ST2 antibody and a pharmaceutical composition. Specifically, this invention relates to an anti-ST2 antibody or its antigen-binding fragment, wherein the anti-ST2 antibody comprises a heavy chain variable region and a light chain variable region, the heavy chain variable region comprising HCDR1 to HCDR3, and the light chain variable region comprising LCDR1 to LCDR3, wherein: the amino acid sequence of HCDR1 is as shown in SEQ ID NO:1, the amino acid sequence of HCDR2 is as shown in SEQ ID NO:2, and the amino acid sequence of HCDR3 is as shown in SEQ ID NO:3; and the amino acid sequence of LCDR1 is as shown in SEQ ID NO:4, the amino acid sequence of LCDR2 is as shown in SEQ ID NO:5, and the amino acid sequence of LCDR3 is as shown in SEQ ID NO:6. The antibody of this invention can effectively bind to human ST2, block the binding of human IL-33 to ST2, and inhibit the activation of downstream signaling pathways in the human IL-33 / ST2 pathway, showing good application prospects.

This invention discloses a pyrrolobenzene derivative compound, its preparation method, and its pharmaceutical application, belonging to the field of chemical pharmaceutical raw materials and formulation manufacturing technology. The compound has the structure shown. This compound specifically binds to the SGLT-2 protein through a pyrrolobenzene conjugated system, inhibiting its glucose transport function and affecting the IC50 of SGLT-2. 50 Values ​​range from 15 to 105 nM. Suitable for preparing drugs to treat non-alcoholic liver disease, solid tumors, hematological malignancies, and autoimmune diseases, especially effective against abnormal glucose and lipid metabolism in hepatocytes and energy deprivation in tumor cells. The compound possesses enhanced metabolic stability due to its deuterated group and can be formulated into tablets, capsules, injections, and other dosage forms.

The application discloses application of SGI-7079 in treating FLT3 mutant acute myeloid leukemia. The application research shows that SGI-7079 can be stably combined with FLT3, inhibit the phosphorylation level of FLT3 and downstream STAT5, AKT and ERK, and induce G1 phase arrest and cell apoptosis. In vitro, SGI-7079 has strong inhibitory effect on FLT3-ITD and drug-resistant mutant cells; in a FLT3-ITD mouse model, SGI-7079 can significantly reduce leukemia load and prolong survival, and shows better curative effect than existing drugs on drug-resistant mutations such as F691L and D835Y. Meanwhile, SGI-7079 also has significant inhibitory effect on primary cells of FLT3-ITD positive patients. It is shown that SGI-7079 can be used as a new drug candidate for treating FLT3 mutation and drug-resistant AML, and provides a new direction for optimizing targeted therapy strategy.

This disclosure pertains to the field of biomedicine, specifically relating to TL1A antibodies and their applications. The antibody or its antigen-binding fragment disclosed herein can bind to TL1A, block the binding of TL1A to DR3, inhibit TL1A-induced TF-1 cell apoptosis, inhibit TL1A-induced NF-κB signaling pathway activation, and inhibit TL1A-induced IFN-γ expression in blood cells.

A recombinant vector, a lentivirus, a lung-exempt MSLN CAR-T cell, and an anti-tumor agent are provided. The recombinant vector includes a first nucleotide sequence, a second nucleotide sequence, and a third nucleotide sequence, the first nucleotide sequence encodes a mesothelin (MSLN)-binding domain, the second nucleotide sequence encodes a leukocyte immunoglobulin-like receptor (LIR-1), and the third nucleotide sequence specifically binds to a lung-highly-expressed molecule. The lentivirus is constructed using the recombinant vector. The lung-exempt MSLN CAR-T cell is constructed using the recombinant vector or the lentivirus. When the lung-exempt MSLN CAR-T cell enters lung tissue, the second nucleotide sequence binds to the lung-highly-expressed molecule through the third nucleotide sequence, inhibiting the killing function of CAR-T to avoid pulmonary toxicity; when the lung-exempt MSLN CAR-T cell infiltrates tumor tissue, the second nucleotide sequence is inactivated, activating CAR-T cells to kill tumor cells, offering the advantages of precise therapy and low side effects.

The present disclosure pertains to compositions, methods, and kits for improving the rate of double-strand break (DSB) repair by homology directed repair (HDR) through inhibition of 53BP1 mediated DNA end protection in combination with inhibition of microhomology-mediated end joining (MMEJ), or alternatively in combination with inhibition of non-homologous end joining (NHEJ), or in combination with inhibition of both MMEJ and NHEJ

Disclosed is use of Raddeanoside R8 in the preparation of a DKK1 inhibitor and a cancer therapeutic drug. Raddeanoside R8 can bind to DKK1 and inhibit the activity of DKK1; moreover, Raddeanoside R8 can inhibit the viability or invasion ability of cancer cells expressing DKK1 proteins.

A specific polypeptide interfering with the binding of Rac1 and PAK2, a pharmaceutical composition thereof and application, the amino acid sequence of the specific polypeptide is shown as SEQ ID NO:1; the polypeptide blocks the binding of Rac1 and the 81-85 amino acids (EHTIH) of PAK2 protein by competitive binding, inhibits the phosphorylation of PAK2 and the activation of downstream TGF-beta, alpha-SMA and collagen I fibrosis pathway. The application discloses a pharmaceutical composition comprising the polypeptide and application of the polypeptide in preparation of a medicine for treating diabetic kidney fibrosis. In vitro cell experiments show that the polypeptide inhibits the increase of p-PAK2 and the expression of fibrosis factors induced by high glucose in vitro; animal experiments show that the polypeptide can improve the pathological damage of the kidney of diabetic mice, reduce the expression of fibrosis-related factors, and has high specificity and long-acting property, thereby providing a new direction and method for the treatment of diabetic kidney fibrosis.

This invention belongs to the field of biomedical engineering technology, specifically relating to the construction and application of a screening model for influenza virus receptor binding inhibitors. Addressing the problem of influenza virus hemagglutinin (HA) being prone to mutation and having multiple subtypes, making it difficult to screen for broad-spectrum inhibitors, this invention replaces HA with elderberry lectin (SNA), which specifically recognizes α-2,6-sialic acid. Using MDCK cells overexpressing α-2,6-sialic acid, a fluorescently labeled high-throughput screening model is constructed by labeling SNA with fluorescein isothiocyanate (FITC). The relative fluorescence units (RFU) of the system are detected using a multifunctional enzyme-linked immunosorbent assay (ELISA) reader. Active compounds inhibit the binding of SNA to cell surface receptors, resulting in a lower RFU value, while inactive compounds show a higher RFU value. This invention provides key technical support for the development of novel inhibitors targeting influenza virus receptor binding.

The present invention addresses the problem of providing an inhibitor of cellular iron uptake targeting TfR, and an inhibitor of binding between human Tf and human TfR. According to the present invention, provided is an inhibitor of cellular iron uptake, said inhibitor comprising an antibody which recognizes the 629th to 633rd amino acids in human transferrin receptor.

This invention relates to the application of hedera saponin A1 in the preparation of drugs for the prevention and / or treatment of seborrheic keratosis or its secondary lesions. Through molecular-level experiments, this invention verifies that hedera saponin A1 can directly bind to the AKT1 protein, inhibiting AKT1-induced upregulation of pro-apoptotic proteins, thereby initiating cell apoptosis. Compared with existing technologies, this invention is a non-invasive treatment, painless, non-invasive, and leaves no scars after healing. Furthermore, this invention has the dual efficacy of "treating seborrheic keratosis" and "chemopreventing malignant transformation." In addition, hedera saponin A1 has a significant killing effect on seborrheic keratosis lesion cells, exhibiting a killing effect on the epidermal layer of isolated seborrheic keratosis lesion tissue, but without inducing significant apoptosis in dermal cells.

This invention discloses the use of cyclic dipeptides in the preparation of drugs for the prevention / treatment of metabolism-related inflammatory diseases, belonging to the field of biomedical technology. The cyclic dipeptide has the following structural formula and molecular formula C1. 18 H 18 N2O2, with a molecular weight of 294.35 Da, is an ADCY7 inhibitor. It inhibits ADCY7 protein expression by binding to ADCY7, thereby playing a role in the prevention / treatment of diseases such as fatty liver associated with metabolic dysfunction. It is composed of natural amino acids, has good biocompatibility, low immunogenicity, and few toxic side effects, and has good safety. It overcomes the defect of easy degradation in vivo of traditional linear peptide drugs and has broad prospects for the development of indications.

The application discloses a biological medicine use of fluvoxamine. The application obtains a series of potential IGSF11 small molecule inhibitors through artificial intelligence assisted virtual screening, wherein, the application first proposes and verifies that fluvoxamine can effectively combine IGSF11, inhibit tumor cell proliferation activity and migration and diffusion capacity, and then realizes effective tumor treatment. Experimental data also shows that fluvoxamine can expand the response rate of PD-1 monoclonal antibody to a certain extent, thereby providing a new selection and direction for clinical treatment of IGSF11 mediated tumors.