39 results about "Lung fibrosis" patented technology

The application discloses application of a PRMT3 inhibitor SGC707 in preparation of a drug for treating pulmonary fibrosis, and for the first time verifies that a selective PRMT3 inhibitor SGC707 can dose-dependently inhibit expression of fibrosis markers such as COL1A1 and alpha-SMA in fibroblasts induced by TGF-beta 1 in vitro; in a bleomycin (BLM) induced mouse pulmonary fibrosis model, SGC707 administration can significantly improve lung tissue collagen deposition, reduce inflammatory cell infiltration, repair alveolar structure damage, and effectively down-regulate expression levels of fibrosis related proteins in lung tissues. It is proved that PRMT3 is a functional target with important intervention value in pulmonary fibrosis, SGC707 has definite anti-pulmonary fibrosis activity in vitro and in vivo, and a new drug strategy is provided for treatment of pulmonary fibrosis.

The present application relates to the technical field of content detection, in particular to a method for rapidly detecting the content of hydroxyproline in mouse lung tissue, which comprises the following steps: obtaining the original sampling spectrum of the lung tissue of the mouse to be detected at different preset sampling points, and obtaining a non-lung tissue interference characteristic base matrix containing whole blood characteristics and cartilage characteristics; setting an orthogonal filter operator and determining a lung interstitium characteristic spectrum vector; constructing a reference spectrum vector and determining a relative spectral response factor; constructing a spectral minimum spanning tree and determining a signal contribution weight based on the spectral minimum spanning tree and the relative spectral response factor; generating a whole lung fibrosis synthetic spectrum according to the signal contribution weight and the lung interstitium characteristic spectrum vector, and detecting the content of hydroxyproline based on the whole lung fibrosis synthetic spectrum. The present application considers the non-lung tissue interference containing whole blood characteristics and cartilage characteristics when detecting the content of hydroxyproline, which improves the rationality of the detection of the content of hydroxyproline to a certain extent.

The application discloses a new use of a BET inhibitor YD-851 or a pharmaceutically acceptable salt thereof in the preparation of a drug for treating pulmonary fibrosis. The application finds that YD-851 can inhibit the expression of BRD4 and fibrosis-related markers in pulmonary fibrosis tissues, reduce the structural damage of bleomycin-induced mouse lung tissues, inflammatory cell infiltration and fibrosis pathological changes, and improve lung function damage. Experimental results show that YD-851 can reduce the pulmonary fibrosis score, inflammation score and area ratio of consolidation, improve the lung imaging abnormalities, and down-regulate the expression of fibrosis-related genes such as Col1a1, Fn1 and Acta2. It is shown that YD-851 has the effect of treating pulmonary fibrosis, and can be used for preparing a drug for treating pulmonary fibrosis, and a new use of YD-851 is developed.

Apparatuses, systems and methods are provided for treating pulmonary tissues via delivery of energy, generally characterized by high voltage pulses, to target tissue using a pulmonary tissue modification system (e.g., an energy delivery catheter system). Example pulmonary tissues include, without limitation, the epithelium (the goblet cells, ciliated pseudostratified columnar epithelial cells, and basal cells), lamina propria, submucosa, submucosal glands, basement membrane, smooth muscle, cartilage, nerves, pathogens resident near or within the tissue, or a combination of any of these. The system may be used to treat a variety of pulmonary diseases or disorders such as or associated with COPD (e.g., chronic bronchitis, emphysema), asthma, interstitial pulmonary fibrosis, cystic fibrosis, bronchiectasis, primary ciliary dyskinesia (PCD), acute bronchitis and / or other pulmonary diseases or disorders.

This application relates to the field of biotechnology, and particularly to Arg1-targeting double-stranded oligonucleotides and their conjugates, pharmaceutical compositions, and their application in pulmonary fibrosis. The Arg1-targeting double-stranded oligonucleotide comprises a sense strand and an antisense strand, wherein the sense strand and antisense strand are at least partially anticomplementary to form a double-stranded region; the nucleotide sequence of the sense strand comprises a sequence differing from the sequence shown in SEQ ID NO.1 by no more than 3 nucleotides, and the nucleotide sequence of the antisense strand comprises a sequence differing from the sequence shown in SEQ ID NO.2 by no more than 3 nucleotides. Using this Arg1-targeting double-stranded oligonucleotide and its conjugates, or pharmaceutical compositions containing it, to reprogram the nucleic acid of M2 macrophages in pulmonary fibrosis can effectively alter their pro-fibrotic functional state.

The present invention relates to the field of cell therapy. Disclosed are a fibroblast activation protein-targeting CAR T-cell, a preparation method therefor, and an application thereof. A CAR T-cell can be prepared by introducing an FAP-targeting chimeric antigen receptor (CAR) into a T lymphocyte, wherein the CAR in the CAR T-cell comprises a signal peptide, an antigen-binding domain, a hinge region, a transmembrane domain, a co-stimulatory signaling region, and a CD3 signaling domain. The CAR T-cell specifically recognizes the FAP by means of a single-chain variable fragment (scFv), which activates an intracellular signaling pathway, releasing cytokine IFN-γ, and exhibiting a cytotoxic effect on FAP+ cells, thereby achieving specific depletion of FAP+ cells at a lesion site. The CAR-T cell can be used for treating diseases characterized by upregulated FAP expression, such as fibrosis (pulmonary fibrosis, hepatic fibrosis, cardiac fibrosis, renal fibrosis, etc.), arthritis, autoimmune disorders (Crohn's disease, rheumatoid arthritis, etc.), and cardiovascular diseases, and demonstrates tremendous application potential and commercial value.

The present application relates to the technical field of medicine, and particularly relates to an anti-pulmonary fibrosis prodrug compound and a preparation method and application thereof. The prodrug compound is a novel prodrug, and the structure comprises: a) an active drug unit selected from pirfenidone and nintedanib; b) a lung targeting unit selected from diphenyl chloroiodonium salt and a mimic thereof 521; and c) a linker unit which is a responsive linkage sensitive to a biomarker specifically overexpressed in a pulmonary fibrosis microenvironment. The prodrug is stable in the systemic circulation and has no activity or low activity, and can be actively targeted to a pulmonary fibrosis lesion; under the specific stimulation of the PFM, the linker is broken, and the original drug molecule is accurately released, so that the concentration of the drug in the lesion site is significantly increased, the toxic side effects caused by systemic exposure are reduced, and the anti-pulmonary fibrosis effect is enhanced.

Provided herein are lung forming progenitor cell therapies which do not require pre-conditioning treatments. Administration of the progenitor cells can replace or replenish populations of host-derived patch forming cells to reverse or inhibit fibrosis, promote healing, and improve lung function. Further disclosed herein are methods for monitoring fibrosis, and for determining whether a subject will be receptive to progenitor cell treatments.

The disclosure herein relates to the development and production of novel antibodies and antigen-binding fragments thereof that bind to TL1A and are useful in the treatment, prevention, and diagnosis of diseases, disorders, or inflammation, including, for example, autoimmune diseases, including rheumatoid arthritis, inflammatory bowel disease, atopic dermatitis, systemic lupus erythematosus, asthma, ulcerative colitis, Crohn's disease, psoriasis, primary biliary cirrhosis, primary biliary cholangitis, ankylosing spondylitis, and fibrosis, including intestinal fibrosis, pulmonary fibrosis, and liver fibrosis. Some of the elements of the final antibody structure are designed de novo by a computer system and its data training set, without reference to a particular reference molecule.

According to various aspects of this disclosure, the present disclosure relates to a method for treating or reducing pulmonary inflammation and / or pulmonary fibrosis in a subject in need thereof comprising intramuscularly administering to the subject a recombinant adeno-associated virus (rAAV) vector. In some aspects, the rAAV vector comprises a vector genome and an AAV capsid (e.g., an AAV1 serotype). In some aspects, the vector genome comprises AAV inverted terminal repeats (ITRs) flanking an expression construct comprising a nucleotide sequence encoding a Fibroblast growth factor 21 (FGF21) or functional fragment thereof operably linked to a ubiquitous promoter.

The application belongs to the technical field of biological medicine, and particularly relates to application of VSIG4 as a biomarker in evaluation of risk of lung fibrosis progression. The application first discovers and verifies that VSIG4 is significantly highly expressed in ILD patients with active inflammatory response, and the high expression is closely related to a signal of continuous progression of the disease by integrating peripheral blood exosome proteomics data and lung tissue single-cell transcriptome data. Based on the discovery, the application provides a kit and a detection method for detecting a VSIG4 protein level in peripheral blood. Data show that the PPF patients can be effectively identified by detecting the content or level of the exosome protein VSIG4 in peripheral blood, and the method has high sensitivity and specificity. The application provides a new non-invasive solution for early risk prediction and disease progression monitoring of lung fibrosis, and has important clinical value.

Disclosed herein are methods of stabilizing or improving lung function in subjects with idiopathic pulmonary fibrosis by orally administering a daily amount of between 1600 mg and 2500 mg deupirfenidone. Also disclosed are methods of dose escalation for initial titration, methods of reducing the incidence of emerging adverse events, and methods of directly transitioning patients from other drugs to deupirfenidone without titration.

The application relates to the technical field of biological medicine, in particular to application of a Setdb1 inhibitor in preparation of a medicine for treating and / or preventing organ fibrosis. The organ includes a heart and a lung, and the application combines in-vitro and in-vivo models to find that knocking out a Setdb1 gene or inhibiting Setdb1 can reduce the levels of heart and lung fibrosis, SETDB1 is expected to become a new target for treating multi-organ fibrosis, and provides a potential treatment scheme for the current situation that there is no specific medicine for treating fibrosis of other organs except the lung.

The present invention provides a combination therapy comprising a TNF inhibitor compound and a mitochondrial complex I modulator (MCIM) compound that is useful in the medical field of inflammatory and progressive disorders such as RA, IBD, idiopathic pulmonary fibrosis, interstitial lung disease, and MS.

The application belongs to the technical field of biological medicine, and particularly relates to a substituted cyano quinolinone compound and a preparation method and application thereof. The substituted cyano quinolinone compound has a significant inhibitory effect on phosphodiesterase type I, has a significant therapeutic effect on animal models of phosphodiesterase related diseases, lung fibrosis, intestinal inflammation and the like, and can be developed into a new target candidate drug for inflammatory diseases such as lung fibrosis and intestinal inflammation. Moreover, the preparation method of the substituted cyano quinolinone compound is simple, the reaction condition is mild, and is very suitable for large-scale industrial production.

This invention provides the use of a trisaccharide compound with a core structure of GlcN(1→4)IdoA(1→4)GlcNS in the preparation of a medicament for treating or preventing pulmonary fibrosis. This medicament can improve pulmonary inflammatory responses, reduce the degree of damage to lung tissue structure, improve or inhibit or delay the progression of pulmonary fibrosis, and ultimately improve and enhance pulmonary ventilation function in patients with pulmonary fibrosis.

Disclosed herein are modulators of a transposable element or a transposable element transcript, wherein the modulators induce or facilitate a cell state transition or change. Further provided herein are synthetic polynucleic acids comprising a nucleic acid sequence of a transposable element or a portion thereof, wherein the synthetic polynucleic acids induce or facilitate cell state transitions or changes. Further provided herein are methods of preventing, alleviating, or treating pulmonary fibrosis in a subject in need thereof. Further provided herein are methods of cellular reprograming and reversing aging in a pulmonary tissue. Further provided herein are methods of diagnosing or prognosing pulmonary fibrosis.

This invention discloses the application of NLRX1 protein inhibitors in the preparation of products with protective effects against pulmonary fibrosis, belonging to the field of biomedical technology. This invention, through the use of an NLRX1 gene knockout mouse model and siRNA silencing technology, demonstrates that inhibiting NLRX1 can significantly alleviate bleomycin-induced pulmonary fibrosis pathological damage. Its protective mechanisms include promoting the proliferation of type II alveolar epithelial cells, inhibiting their damage and apoptosis, and reducing myofibroblast infiltration and extracellular matrix deposition. Based on this, this invention provides for the first time a therapeutic strategy targeting the inhibition of the NLRX1 protein. Related products include recombinant vectors containing RNA molecules encoding NLRX1 expression inhibitors or other drugs capable of inhibiting NLRX1 expression. This invention provides new targets and drug development directions for the treatment of fibrotic diseases, especially pulmonary fibrosis.

The present invention relates to novel Collagen 1 translation inhibitors, composition and methods of preparation thereof, and uses thereof for treating Fibrosis including lung, liver, kidney, cardiac and dermal fibrosis, IPF, wound healing, scarring and Gingival fibromatosis, Systemic Sclerosis, and alcoholic and non-alcoholic steatohepatitis (NASH).

The present disclosure provides compounds of the formula: for use in the treatment of systemic sclerosis, fibrosis (e.g. pulmonary fibrosis), achondroplasia, thanatophoric dysplasia (e.g. type I), severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN), muenke syndrome or cancer.

The invention relates to the technical field of medicines, in particular to application of massoia lactone in preparation of an anti-pulmonary fibrosis medicine.

Nano-entity compositions composed of a plurality of self-associated compounds of Formula 1 and / or Formula 2, for example, 2-[(Z)-[l-(2-amino-l,3-thiazol-4-yl)-2-oxo-2-(2-oxoethylamino)ethylidene]amino]oxyacetic acid, where R1 is a carboxylic acid group and R2 is an amine group, have antifibrotic properties, effective for inhibiting type I collagen synthesis by inhibiting binding of LARP6 with a 5' stem-loop of a collagen mRNA. The described nano-entity compositions may be used in a method of treating a patient having a fibrotic condition, including but are not limited to a pulmonary fibrosis, a liver fibrosis, a heart fibrosis, a circulatory system fibrosis, a skin fibrosis, a renal fibrosis, and / or an intestinal fibrosis.

This invention discloses the application of PRDM16 or a truncated variant thereof in the preparation of drugs for the prevention and / or treatment of pulmonary fibrosis, belonging to the field of biomedicine. This invention discovers that PRDM16 can inhibit fibroblast activation and screens for a truncated variant of PRDM16 capable of treating pulmonary fibrosis via adeno-associated virus (AAV). Therefore, this invention provides the application of PRDM16 or a truncated variant thereof in the preparation of drugs for the prevention and / or treatment of pulmonary fibrosis, wherein the truncated variant of PRDM16 is PRDM16 lacking the PR domain. △PR PRDM16 may be missing the PR and ZF1 domains. △PR‑ZF1 This invention provides new ideas and effective solutions for delaying or reversing the further development of pulmonary fibrosis.

This disclosure provides the use of a farnesoid X receptor (FXR) agonist in the preparation of a medicament for the prevention or treatment of pulmonary fibrosis. This disclosure demonstrates, both in vivo and in vitro, the anti-pulmonary fibrosis activity of the clinical-stage farnesoid X receptor (FXR) compound.

This invention discloses a PDE4 inhibitor, its preparation method, and its applications, belonging to the field of pharmaceutical technology. Targeting PDE4, this invention designed and synthesized 36 novel PDE4 inhibitors. The synthesized PDE4 inhibitors exhibit significant inhibitory effects on PDE4, and most compounds possess anti-inflammatory activity. Compound 11b has been shown to have therapeutic effects on pulmonary fibrosis.

This invention discloses the application of eugenol in the preparation of drugs for the treatment of tissue fibrosis. This invention is the first to propose and verify that eugenol can inhibit ferroptosis in lung epithelial cells, thereby inhibiting the migration of fibroblasts and downregulating the expression of fibrosis-related proteins, thus effectively alleviating the progression of fibrosis and providing a new direction for the treatment of tissue fibrosis, especially pulmonary fibrosis.

This invention relates to extracellular vesicles derived from human mesenchymal stem cells and their use. The extracellular vesicles derived from mesenchymal stem cells according to the present invention inhibit the expression of fibrosis-related proteins, wound closure, and cell infiltration, which are increased in lung epithelial cells due to TGF-β1 treatment. In addition, microRNAs contained in large quantities in the extracellular vesicles inhibit the gene expression of fibrosis-related proteins in lung epithelial cells and lung fibroblasts. These extracellular vesicles significantly reduce the expression of fibrosis-related proteins, collagen production, and fibrotic areas in a mouse model of pulmonary fibrosis. Therefore, the extracellular vesicles according to the present invention can be used to prevent and treat pulmonary fibrosis.

The present invention relates to a formulation in particular an oral formulation for the prophylaxis and treatment of TG2-related disorders like fibrosis in particular diabetic nephropathy and / or diabetic associated non-alcoholic steatohepatitis (NASH) and / or non-alcoholic steatohepatitis, and its use in the prophylaxis and / or treatment of fibrosis in particular nephropathy, NASH, idiopathic pulmonary fibrosis, and cystic fibrosis. Further, the present application relates also to the use of (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1H-imidazole-5-carboxamido)-7-oxohept-2-enoate as hepatoprotectant, i.e. as hepatoprotective agent. In addition the present invention relates to a pharmaceutical composition comprising (S,E)-methyl-7-(1-(2-(2-ethylbutylamino)-2-oxoethyl)-2-oxo-1,2-dihydro-pyridin-3-ylamino)-6-(1-methyl-1H-imidazole-5-carboxamido)-7-oxohept-2-enoate for use as hepatoprotective agent and for use in the protection of the liver against liver toxicity, the improvement of liver function, and / or in the prophylaxis or treatment of a liver disease or liver disorder.

A novel strain, Lactobacillus paracasei ATG-E1 (Accession No. KCTC 14245BP), and a composition containing the same for preventing or treating respiratory diseases which are caused by fine particulate matter. The Lactobacillus paracasei ATG-E1 strain reduces the number of immune cells bronchoalveolar and lung tissues and inhibits the expression of inflammatory cytokines such as interleukin-17A (IL-17A), tumor necrosis factor-α (TNF-α), macrophage inflammatory protein 2 (MIP2), C-X-C motif chemokine ligand 1 (CXCL-1), macrophage inflammatory protein-α (MIP-1α) or interleukin-6 (IL-6). Therefore, the Lactobacillus paracasei ATG-E1 strain can be used for a treatment or health functional food for various respiratory diseases such as acute and chronic bronchitis, catarrhal bronchitis, bronchitis obliterans, inflammatory bronchitis, bronchial asthma, atopic asthma, non-atopic asthma, atopic IgE-mediated asthma, allergic asthma, non-allergic asthma, chronic bronchoconstriction, acute bronchoconstriction, chronic obstructive pulmonary disease, bronchial adenoma, pulmonary tuberculosis, emphysema, lung abscess, pulmonary fibrosis, lung cancer, airway cancer, bronchoalveolar cancer, and bronchial cancer.

This invention relates to the application of tanshinone A ester derivatives with carbon chain lengths of C1-C2, as shown in Formula I, in the preparation of drugs for treating idiopathic pulmonary fibrosis. This invention systematically investigated the oral absorption behavior of tanshinone A ester derivatives of different carbon chain lengths in rats, and confirmed through in vitro HFL1 cell models and in vivo bleomycin-induced pulmonary fibrosis mouse models that these short-chain ester derivatives (methyl and ethyl esters) can significantly improve oral bioavailability and inhibit TGF-β1-induced α-SMA expression and extracellular collagen deposition, demonstrating significantly superior characteristics compared to the original tanshinone A and its long-chain ester derivatives. Most importantly, cytotoxicity experiments showed a significantly improved safety profile, demonstrating an excellent therapeutic window. This invention overcomes the shortcomings of low bioavailability and well-defined toxicity of tanshinone A in existing technologies, providing a more efficient and safer new drug option for the treatment of idiopathic pulmonary fibrosis.