397 results about "Lung fibrosis" patented technology

The present disclosure provides methods of treating pulmonary fibrosis, the methods comprising administering taladegib to a subject in need thereof.

The present disclosure provides methods of treating pulmonary fibrosis, the methods comprising administering taladegib to a subject in need thereof.

The present specification provides methods and compositions for treating fibrosis, particularly pulmonary fibrosis. The pulmonary fibrosis may be idiopathic or arise following an infection of the lung. The lung infection can be by SARS-COV-2. Lung function stabilizes or is improved as a result of treatment.

The present disclosure provides methods of treating pulmonary fibrosis, the methods comprising administering taladegib monotherapy as the main component to a subject in need thereof, as well as diagnostic criteria and markers establishing the progress of therapy.

The invention discloses a radionuclide labeled molecular probe for detecting collagen structure denaturation and a preparation method and application thereof, and relates to the technical field of biology. The structural general formula of the radionuclide labeled molecular probe disclosed by the invention is as follows: K (chelating agent-nuclide)-K-Linker-CHP, wherein K (chelating agent-nuclide) is a lysine residue labeled by a side chain amino coupling chelating agent and a radionuclide; the Linker is a connection joint; cHP is a collagen hybrid peptide with a polypeptide sequence of (GfO) n or (GPO) n. The probe has excellent definition and signal-to-noise ratio, not only can detect pancreatic ductal adenocarcinoma in a pancreatic cancer model, but also can sensitively detect precancerous lesions (such as pancreatic intraepithelial neoplasia lesions) of the pancreatic ductal adenocarcinoma and pulmonary fibrosis lesions in a bleomycin pulmonary fibrosis model. And the kit has important significance on early detection of pancreatic duct adenocarcinoma and reflection of dynamic change of ECM remodeling.

The invention belongs to the field of pharmacy, and relates to a medicine for treating pulmonary fibrosis, in particular to application of an anti-Gremlin1 antibody to preparation of a medicine for preventing and treating pulmonary fibrosis. The Gremlin1 antibody disclosed by the invention can be applied to prevention and treatment of pulmonary fibrosis, effectively improves bleomycin (BLM)-induced pulmonary fibrosis lesions of mice and improves the survival rate of the mice. Compared with a BLM group, the mouse inspiration capacity (IC) and the lung static compliance (CRS) treated by the Gremlin1 antibody are remarkably improved, the hydroxyproline content in lung tissue is remarkably reduced, and compared with the BLM group, the Ashcroft score, the collagen deposition area in Masson three-color dyeing and the Sirius red dyeing area of an antibody intervention group are remarkably reduced, and the proportion of activated endothelial cells and the proportion of transition-state epithelial cells are remarkably reduced. Therefore, the Gremlin1 antibody can be used for preparing the medicine for preventing and / or treating the pulmonary fibrosis.

Disclosed is a method for ameliorating, preventing or treating systemic sclerosis and pulmonary fibrosis, including administering to a subject in need thereof a composition containing Bifidobacterium longum RAPO (KCTC13773BP) as an active ingredient. The composition controls infiltration and inflammatory response of inflammatory monocytes and macrophages, and facilitates an increase in short-chain fatty acid producing microorganisms, thus being effective in ameliorating, preventing or treating systemic sclerosis and pulmonary fibrosis.

The present disclosure provides methods of treating pulmonary fibrosis, the methods comprising administering taladegib to a subject in need thereof.

The invention relates to application of hydroxynidone to preparation of a medicine for preventing and / or treating radiation-induced pulmonary fibrosis. Pharmacological experiments prove that the hydroxynidone has a definite resisting effect on radioactive rat lung injury including early inflammatory exudation and pulmonary interstitial fibroblast hyperplasia, and can obviously reduce pulmonary alveolar inflammatory cell exudation and reduce the content of TGF beta 1 in inflammatory exudate; the medium and large doses have the effect of delaying the development of interstitial pneumonia towards pulmonary fibrosis; the lesion degrees of the small, medium and large dosage groups are obviously reduced and are in a dose-effect relationship.

The invention discloses a tetrandrine ferulate and its application in the preparation of a medicament for treating pulmonary fibrosis. The pharmacological effects of tetrandrine and ferulic acid, as well as those after salification, are studied. It is found that both have an anti-pulmonary fibrosis effect, and the two can be used in combination to synergistically exert a more excellent anti-pulmonary fibrosis efficacy. At the same time, the solubility of tetrandrine can also be increased. This has not been reported in existing literature. The tetrandrine ferulate of the present invention has lower cytotoxicity, and the cell viability of normal human liver cells LO-2 and human embryonic fibroblasts MRC-5 is higher than that of tetrandrine, which alleviates the burden of liver and lungs to a certain extent and has good safety.

The invention relates to the technical field of biological medicines, in particular to application of 1, 3-butanediol in treatment of idiopathic pulmonary fibrosis. 1, 3-butanediol inhibits pulmonary fibrosis and promotes lung function recovery by regulating AT2 cell proliferation, inhibiting differentiation of fibroblasts to myofibroblasts, inhibiting polarization of macrophages to M2 macrophages and regulating lipid metabolism.

The present disclosure provides methods of treating pulmonary fibrosis, the methods comprising administering taladegib to a subject in need thereof.

The invention discloses a liposome targeting lung macrophages, the liposome is of a double-layer self-assembly structure, the particle size is more than 1 [mu] m, and the liposome comprises SPC, DOTAP, DSPE-PEG2000-mannose and cholesterol. The liposome has efficient targeting property, and the loaded Kdm6a mRNA can recover the expression of KDM6A in macrophages and inhibit the secretion of THBS1, so that the glycerophospholipid metabolism of ATII cells is repaired, the pulmonary fibrosis is improved, and the treatment effect is remarkable.

The disclosure relates to compounds of the disclosure and pharmaceutically acceptable salts thereof to their use in medicine; to compositions containing them; to processes for their preparation; and to intermediates used in such processes. The compounds of the disclosure may be useful in the treatment, prevention, suppression and amelioration of disease(s) such as atopic dermatitis, eosinophilic gastritis, atopic keratoconjunctivitis, allergy, alopecia, Alzheimer's disease, asthma, atherosclerosis, Bechet's disease, bullous pemphigoid, cancer, chronic obstructive pulmonary disease, chronic pruritis, chronic urticaria, Crohn's disease (CD), dermatitis, diabetic kidney disease, eosinophilic esophagitis, fungal keratitis, gout, idiopathic pulmonary fibrosis (IPF), keloids, non-alcoholic steatohepatitis (NASH), primary biliary cirrhosis, prurigo nodularis, psoriasis, psoriatic arthritis, rhinosinusitis, scleroderma, systemic lupus erythematosus (SLE), systemic sclerosis, ulcerative colitis (UC), vitiligo, or hidradenitis suppurativa. The compounds of the disclosure may be useful in the treatment, prevention, suppression and amelioration of a dermatological condition or a respiratory condition.

The present invention relates to FGFR3 inhibitor compounds of novel structure or pharmaceutically acceptable salts, isotope variants, tautomers, stereoisomers or prodrugs thereof, and their use as medicine. The compounds are useful in the treatment of cancers such as urothelial carcinoma, systemic sclerosis, fibrosis, pulmonary fibrosis, cartilage insufficiency, lethal insufficiency, severe cartilage insufficiency accompanied by developmental retardation and atrachis ossicular, or muenke syndrome. # imgabs0 #

Disclosed herein are double stranded ribonucleic acids (dsRNAs) and synthetic antisense oligonucleotides (ASOs) for use in inhibiting the expression of MUC5B and in the treatment of a subject having a disease or disorder characterized by overexpression of MUC5B, including in subjects having lung disease or in a subject at risk of developing lung disease, for example, in a subject having or at risk of developing idiopathic pulmonary fibrosis.

The present invention relates to immunoassays for detecting the whole endotrophin peptide. The assay can be used to detect and / or monitor a disease in a patient and / or assessing the likelihood of, or the severity of a disease in a patient. The disease may be selected from cardiovascular disease, idiopathic pulmonary fibrosis (IPF) or chronic kidney disease. The cardiovascular disease may in particular be heart failure, and especially heart failure with preserved ejection fraction. The immunoassay may be for assessing the likelihood of adverse outcomes of the cardiovascular disease, chronic kidney disease and all cause mortality.

The invention relates to the technical field of organoid culture, in particular to a pulmonary fibrosis organoid model and a construction method and application thereof. The pulmonary fibrosis organ-like model is obtained by co-culturing lentivirus stably transfected alveolar epithelial cells, human embryonic lung fibroblasts MRC-5 and macrophages. According to the invention, macrophages are innovatively introduced, a ternary co-culture system of lentivirus stably transfected alveolar epithelial cells, human embryonic lung fibroblasts MRC-5 and macrophages is constructed, and a key'epithelial injury-immune infiltration-fibroblast activation 'pathological triangle in a pulmonary fibrosis pathogenesis process can be more comprehensively simulated; the finally obtained pulmonary fibrosis organ-like model provides an efficient tool for pulmonary fibrosis mechanism research and research, development and screening of anti-pulmonary fibrosis drugs.

Provided is a use of a Galectin-1 inhibitor in preparation of a drug for treating pulmonary fibrosis. Taking silicosis model mice as a subject, administration of a Galectin-1 inhibitor OTX008 to silicosis mice can effectively alleviate the progression of pulmonary fibrosis. Studies have shown that the lung function of mice with silicosis is improved significantly; transcription levels of inflammatory factors Il-1β and Il-6 in the lung tissue of silicosis mice are decreased, concentrations of IL-1β and IL-6 in the alveolar lavage fluid are also decreased, and the infiltration of inflammatory cells is decreased. In the lung tissue of silicosis mice, the transcription levels of fibrosis factors Col-I and Fn-1 are decreased, the collagen-specific amino acid hydroxyproline is decreased, the fibrosis lesions are decreased, and the degree of lesions is alleviated. Therefore, the Galectin-1 inhibitor can be used as a new treatment strategy for pulmonary fibrosis.

The present invention provides, in part, a novel small molecule PHD inhibitor having a structure according to Formula (A) or a sub-formula thereof: or a pharmaceutically acceptable salt thereof. The compounds provided herein are useful in the treatment of diseases, including heart diseases (e.g., ischemic heart disease, congestive heart failure, and valvular heart disease), lung diseases (e.g., acute lung injury, pulmonary arterial hypertension, pulmonary fibrosis, and chronic obstructive pulmonary disease), liver diseases (e.g., acute liver failure and liver fibrosis, and cirrhosis), and kidney diseases (e.g., acute liver failure, liver fibrosis, and cirrhosis). Acute kidney injury and chronic kidney disease).

The invention belongs to the technical field of biological medicine, and discloses application of a Furin inhibitor in preparation of a medicine for preventing, delaying or treating idiopathic pulmonary fibrosis, the effect of the Furin inhibitor in inhibiting generation of P61-Sema3E so as to delay the idiopathic pulmonary fibrosis is found for the first time, the key effect of Furin and P61-Sema3E in generation and development of IPF is further determined, and the application of the Furin inhibitor in preparation of the medicine for preventing, delaying or treating the idiopathic pulmonary fibrosis is provided for the first time. And a new target can be provided for prevention and treatment of IPF. The invention determines that the Furin inhibitor inhibits activation, proliferation and migration of human primary lung fibroblasts by inhibiting the enzyme activity of Furin, reducing the conversion from P87-Sema3E to P61-Sema3E and reducing the generation of P61-Sema3E, so that a new treatment strategy is provided for IPF.

The invention discloses an application of samidocardone in preparation of a medicine for treating pulmonary fibrosis. According to the application disclosed by the invention, the condition that the samidojun can inhibit the activity of the pulmonary fibrosis cells and reduce proliferation by inducing the ferroptosis of the pulmonary fibrosis cells is proposed and verified for the first time, and meanwhile, the expression of fibrosis-related proteins is reduced, so that the progress of the pulmonary fibrosis is effectively relieved, and a new direction is provided for treating the pulmonary fibrosis.

The application relates to application of a sesquiterpenoid compound in preparation of a medicine for preventing and / or treating pulmonary fibrosis. The sesquiterpenoid compound has obvious inhibiting collagen deposition effect on TGF-beta 1 induced human embryo lung fibroblasts, does not show cytotoxicity, has good anti-pulmonary fibrosis activity, and can be used for preparing the medicine for preventing and / or treating pulmonary fibrosis.

The invention relates to the field of pharmaceutical compositions, in particular to a nintedanib-containing pharmaceutical composition or pharmaceutical composition for resisting progressive fibrotic interstitial lung disease (PF-ILD), which comprises a therapeutically effective amount of nintedanib or pharmaceutically acceptable salts, stereoisomers, solvates, prodrugs or derivatives of nintedanib, or pharmaceutically acceptable salts, stereoisomers, solvates, prodrugs or derivatives of nintedanib, or pharmaceutically acceptable salts, stereoisomers, solvates, prodrugs or derivatives of nintedanib. Optionally a pharmaceutically acceptable carrier; the composition has a synergistic inhibition effect on lung fibroblast proliferation through combined administration, can be applied to PF-ILD through inhalation combined administration or prepared into a fixed-dose inhalation compound preparation, especially to patients with idiopathic pulmonary fibrosis (IPF), and aims to solve the problems that the treatment effect is insufficient and the treatment effect is poor in the prior art. The safety and the tolerance are poor.

The invention provides a lung tissue sustained and controlled release material loaded with BMP4 and GANT61 and a preparation method of the lung tissue sustained and controlled release material, and relates to the technical field of disease treatment and delivery materials. The invention relates to a preparation method of a lung tissue sustained and controlled release material loaded with BMP4 and GANT61. The preparation method comprises the following steps: synthesizing HPG by adopting an anionic ring-opening polymerization method; the preparation method comprises the following steps: mixing HPG with PLA, and reacting to prepare a copolymer PLA-HPG; the copolymer PLA-HPG and GANT61 are blended and subjected to a reaction, and nano particles loaded with GANT61 are prepared; and the GANT61-loaded nano particles and BMP4 are subjected to a mixed reaction, such that the BMP4 and GANT61-loaded lung tissue sustained and controlled release material is prepared. The invention constructs a lung tissue sustained and controlled release material loaded with BMP4 and GANT61, and verifies that the lung tissue sustained and controlled release material can realize an anti-pulmonary fibrosis treatment strategy by inducing alpha-SMA + myofibroblast transdifferentiation, resisting inflammation, resisting oxidation and other multiple targets.

The present invention provides a fusion protein composed of an anti-human CTGF antibody and the extracellular domain of the human type II TGF-β receptor, linked via a linker. This fusion protein can bind both CTGF and TGF-β. This fusion protein can be purified in a single step to obtain a 100% pure target protein. Experiments have shown that even a low dose of 1 mg / kg can significantly reduce the degree of pulmonary fibrosis in experimental animals.

The invention discloses a pharmaceutical composition for treating pulmonary fibrosis complicated with depression and application of the pharmaceutical composition, and belongs to the field of biological medicine. The pharmaceutical composition provided by the invention comprises harmine and deoxyvasicine, wherein the optimal mass ratio of harmine to deoxyvasicine is 1: 1.25. The curative effect of the pharmaceutical composition is verified by constructing a pulmonary fibrosis and depression combined mouse model, and experimental results show that the pharmaceutical composition provided by the invention can significantly improve the anti-fibrosis effect, can also effectively reduce the neurotoxicity of harmine, shows a synergistic effect, and can be used for preparing anti-fibrosis drugs for treating or preventing the fibrosis. And the curative effect and the safety are both improved. The invention lays a foundation for developing a safe and efficient novel medicine for treating pulmonary fibrosis combined with depression, and has important application value and wide application prospect in treatment of patients with pulmonary fibrosis combined with depression.

To provide a type C natriuretic peptide and a method for treating acute lung injury. [Solution] This disclosure relates to the treatment of lung, liver, and / or kidney disorders by administering therapeutically effective doses of (ultra)long-acting C-type natriuretic peptide (CNP), CNP derivatives, (ultra)long-acting CNP derivatives, or (ultra)long-acting CNP receptor (NPRB) agonists to subjects in need. This disclosure also relates to the treatment of non-cardiovascular causes of hypoxia, elevated inflammatory cell levels in the lungs, pulmonary edema, sepsis, bacteremia, fibrosis in general, and / or interstitial lung disease using these.

The present invention relates to a combination therapy of pexidartinib and nintedanib for use in the prevention or treatment of pulmonary fibrosis, in particular to a combination therapy of pexidartinib and nintedanib for use in the prevention or treatment of pulmonary fibrosis.

The invention discloses application of an MCP-3 inhibitor in preparation of a medicine for preventing and treating idiopathic pulmonary fibrosis, and belongs to the technical field of biological medicine. The core effect of MCP-3 secreted by lung fibroblasts in the IPF process is disclosed for the first time, and it is found that MCP-3 activates an MEK-ERK pathway through binding to a receptor, promotes inflammatory aging of lung fibroblasts and transdifferentiation to myofibroblasts, and finally causes collagen deposition. Experiments also prove that the MCP-3 inhibitor Bindarit can be used as a novel therapeutic drug to intervene the IPF process and inhibit lung fibroblast aging and transdifferentiation of lung fibroblast to myofibroblast, a new way is provided for clinical treatment of IPF, and the problems of poor curative effect and large side effect of the current drug for clinically treating IPF are solved.