70 results about "Cardiomyopathy" patented technology

The present disclosure provides a method of treating cardiomyopathy and / or related heart failure in a human subject (e.g., an adult human subject) in need of such treatment with 2-(3,5-dichloro-4-((5-isopropyl-6-oxo-1,6-dihydropyridazin-3-yl)oxy)phenyl)-3,5-dioxo-2,3,4,5-tetrahydro-1,2,4-triazine-6-carbonitrile (resmetirom) or a pharmaceutically acceptable salt thereof. The present disclosure also provides a method of treating portal hypertension in a human subject (e.g., an adult human subject) in need of such treatment with 2-(3,5-dichloro-4-((5-isopropyl-6-oxo-1,6-dihydropyridazin-3-yl)oxy)phenyl)-3,5-dioxo-2,3,4,5-tetrahydro-1,2,4-triazine-6-carbonitrile (resmetirom) or a pharmaceutically acceptable salt thereof. The present disclosure also provides a method of treating clinically significant portal hypertension (CSPH) in a human subject (e.g., an adult human subject) in need of such treatment with 2-(3,5-dichloro-4-((5-isopropyl-6-oxo-1,6-dihydropyridazin-3-yl)oxy)phenyl)-3,5-dioxo-2,3,4,5-tetrahydro-1,2,4-triazine-6-carbonitrile (resmetirom) or a pharmaceutically acceptable salt thereof.

This invention discloses the application of alismazone B acetate in the preparation of drugs for the prevention or treatment of hypertrophic cardiomyopathy and its related symptoms. This invention is the first to propose the use of alismazone B acetate (AB23a) for the prevention or treatment of hypertrophic cardiomyopathy. The invention utilizes AB23a to directly treat cardiomyocytes obtained from directed differentiation of human embryonic stem cells in vitro, finding that AB23a treatment significantly inhibits the hypertrophic phenotype of human embryonic stem cell-cardiomyocytes. Feeding mice with hereditary hypertrophic cardiomyopathy caused by gene mutations to a diet containing AB23a showed that AB23a significantly alleviated pathological myocardial hypertrophy and improved cardiac function in mice. AB23a can be used to prepare drugs against hereditary hypertrophic cardiomyopathy, providing a new approach and method for treating hypertrophic cardiomyopathy. AB23a is the most important medicinal component of the traditional Chinese medicine Alisma plantago-aquatica, is safe for organisms, and has good clinical application prospects.

Quinazoline dione compounds are provided for treating cardiac indications such as hypertrophic cardiomyopathy and diastolic dysfunction. Diseases treated by the methods described herein include, but are not limited to, cardiomyopathy, hypertrophic cardiomyopathy (HCM), abnormal heart rhythms, aortic disease, Marfan syndrome, coronary artery disease, heart attack, heart failure, rheumatic heart disease, peripheral vascular disease, stroke, deep vein thrombosis, and pulmonary embolism.

The present invention relates to Givinostat hydrochloride monohydrate for use in the treatment of arrhythmogenic cardiomyopathy.

The application belongs to the technical field of molecular biology, and particularly relates to metabolic markers for evaluating the prognosis of patients with hypertrophic cardiomyopathy and application thereof. The application determines that one or more of 3-hydroxyrilotene, asparagine-lysine, cyclohexylamine, arachidonic acid, aconitic acid, propionyl carnitine, ceramide, tryptophan, 3-hydroxysebacic acid, traumatic acid, phosphatidylcholine, alanine-proline, lysophosphatidylcholine, taurine and S-garlicin cysteine are related to the prognosis of hypertrophic cardiomyopathy, can evaluate the prognosis of patients with hypertrophic cardiomyopathy after undergoing muscle resection of interventricular septum, and shows accurate judgment on all-cause death or rehospitalization, cardiovascular events and postoperative new-onset arrhythmia. Finally, all the prognostic biomarkers are reproduced in an independent cohort, which is helpful for postoperative risk evaluation of patients with hypertrophic cardiomyopathy, has high specificity and high sensitivity.

The application provides a traditional Chinese medicine and diet dispensing device for diabetic cardiomyopathy patients, and relates to the technical field of diet dispensing equipment. The device comprises a box body, a storage area, a discharge area and a receiving area are arranged in the box body from top to bottom; the storage area is composed of multiple storage cavities, the discharge area is provided with a spiral conveying and discharging mechanism, the receiving area is provided with a weighing receiving structure, and a self-cleaning mechanism and a control system are further arranged. The device can realize quantitative storage, automatic discharge, accurate weighing and integrated dispensing of various medicinal and edible materials, and meets the needs of traditional Chinese medicine and diet formula of diabetic cardiomyopathy patients; the self-cleaning mechanism can complete internal flushing, avoid food residue pollution and ensure health safety. The overall structure is compact, the control is accurate and the operation is convenient, which can effectively improve the standardization and automation level of traditional Chinese medicine and diet dispensing, and solve the problems of low efficiency, inaccurate measurement and cross contamination in manual dispensing.

The application belongs to the technical field of molecular biology, and particularly relates to metabolic markers for distinguishing hypertrophic cardiomyopathy and left ventricular hypertrophy and application. The application analyzes the metabolome of hypertrophic cardiomyopathy (HCM) patients, left ventricular hypertrophy (LVH) patients caused by non-hypertrophic cardiomyopathy and healthy people, finds that carnitine C16:2, carnitine C14:0, carnitine C16:0, carnitine C18:0 and carnitine C18:1 are differentially expressed in HCM patients and LVH patients, pyridoxine phosphate, ito acid, adenosine monophosphate, adenosine diphosphate and adenosine triphosphate are differentially expressed in HCM patients and healthy people, lysine base, methyl glutamic acid, acetyl proline, malate semialdehyde and citramalate are differentially expressed in LVH patients and healthy people, and ROC curve analysis shows excellent prediction effect, strong specificity and high sensitivity.

Provided herein are anti-Activin E antibodies having specific complementarity determining regions (CDRs) for the heavy and light chains, heavy and light chains, antigen binding fragments thereof, polynucleotides that encode the same, vectors, and host cells, and methods for treating a metabolic disorder, type 2 diabetes, obesity, an elevated triglyceride level, lipodystrophy, liver inflammation, fatty liver disease, hypercholesterolemia, an elevated liver enzyme, nonalcoholic steatohepatitis (NASH), a cardiovascular disease, cardiomyopathy, high blood pressure, and / or heart failure with the anti-Activin E antibodies disclosed herein.

The disclosure relates to RNAi constructs, such as siRNA, for reducing expression of the TTR gene. Methods of using such RNAi constructs to treat or prevent cardiac disease, such as transthyretin-associated cardiomyopathy (ATTR-CM), are also described.

This application relates to the biomedical field and discloses a combination of biomarkers based on mitochondrial oxidative stress for the auxiliary diagnosis of dilated cardiomyopathy and its application. The biomarker combination includes the TARS2, NOX4, and SNCA genes. This biomarker combination can be used to prepare auxiliary diagnostic kits for dilated cardiomyopathy. By detecting the expression levels of each gene in the biomarker combination, the auxiliary diagnosis of dilated cardiomyopathy can be achieved efficiently and accurately. Compared with traditional diagnostic methods, this application, based on the characteristics of mitochondrial oxidative stress-related genes, has higher diagnostic accuracy and better applicability.

The present invention relates to a compound of formula (I) as inhibitors of calcium calmodulin dependent protein kinase 2 (CAMK2) for the treatment of for the treatment of heart failure, fibrosis, cardiomyopathies, atrial fibrillation, catecholaminergic polymeric ventricular tachycardia, heart block, cardiac arrhythmias, contraception, anxiety, post-traumatic stress disorder, hypertension, tachycardia, diabetes, allergy, and asthma.

This invention relates to the field of biomedical technology, specifically to the application of PTPRM in the treatment and / or prevention of septic cardiomyopathy. This application found that the expression level of PTPRM was significantly reduced in the cardiac tissue of a CLP model, and further verified that overexpression of PTPRM significantly improved the survival rate of the CLP model. Furthermore, the reduction in PAT caused by CLP modeling, as well as the increases in RVDFW, RVSFW, LVSFW, LVDFW, IVS-s, and IVS-d, were also improved. In addition, overexpression of PTPRM can also reduce the expression level of cardiac troponin (cTNT) and right ventricular wall thickness. Therefore, PTPRM can be used as a target for the treatment of septic cardiomyopathy.

The present invention relates to a compound of formula (I) as inhibitors of calcium calmodulin dependent protein kinase 2 (CAMK2) for the treatment of for the treatment of heart failure, fibrosis, cardiomyopathies, atrial fibrillation, catecholaminergic polymeric ventricular tachycardia, heart block, cardiac arrhythmias, contraception, anxiety, post-traumatic stress disorder, hypertension, tachycardia, diabetes, allergy, and asthma.

The present invention relates to methods and compositions for diagnosing and effecting treatment of cardiomyopathy (CM) in felines. In one embodiment, a method of diagnosing CM in a feline can comprise measuring an amount of at least one metabolite from the feline; comparing the amount of the at least one metabolite from the feline to a corresponding predetermined value or a corresponding predetermined range; and diagnosing the feline as preclinical CM, clinical CM, or not having CM based on the comparison.

The application belongs to the field of genetic engineering, and particularly relates to a polynucleotide construct capable of expressing LMNA and application thereof in preventing and treating DCM. The synthetic intron in the application comprises: I) a nucleotide sequence as shown in SEQ ID No. 8, II) a nucleotide sequence having at least one mutation in the 1-8th position of the sequence shown in SEQ ID No. 8, or a nucleotide sequence having at least 90% homology with the sequence shown in I) or II). By using the synthetic intron in the application, two proteins can be simultaneously expressed through alternative splicing, and the ratio of the two proteins or the expression of a single protein can be regulated through mutation of the splicing signal. Compared with the existing gene therapy method for dilated cardiomyopathy caused by LMNA mutation, the expression vector for simultaneously expressing Lamin A and Lamin C proteins in the application has stronger rescue effect.

This invention belongs to the pharmaceutical field and relates to the application of nikkomycin in the preparation of drugs for treating lipid storage myopathy. This invention discloses the use of nikkomycin in the treatment of lipid storage myopathy, particularly in the treatment of simple myopathic neutral lipopathy caused by PNPLA2 gene mutations. Simple myopathic neutral lipopathy is an autosomal recessive, progressive lipid storage myopathy affecting multiple systems throughout the body. Currently, there is no treatment available, and patients develop fatal symptoms such as generalized muscle weakness and cardiomyopathy in the late stages. This invention discovers that nikkomycin can significantly reverse lipid droplet deposition in fibroblasts of patients with simple myopathic neutral lipopathy, reduce inflammatory responses, improve autophagy inhibition, and increase energy production. It can serve as an effective ingredient for treating this disease and has clear application prospects in patients with untreatable simple myopathic neutral lipopathy.

The application provides a multi-modal data fusion evaluation and prognosis prediction method and system for septic cardiomyopathy, which comprises the following steps: obtaining target data and electronic medical records of septic cardiomyopathy patients, combining the target data with a preset first database to construct a correlation matrix; constructing a second database corresponding to the septic cardiomyopathy patients according to the electronic medical records; generating a target interaction path based on the second database; obtaining a first signal according to the causal effect intensity of each node in the target interaction path, and generating a prognosis prediction scheme in combination with a target risk threshold. The application realizes real-time tracking and closed-loop intervention of the pathological process of septic cardiomyopathy, and fundamentally solves the prognosis prediction deviation caused by the time and space disconnection of the traditional database.

The present disclosure relates to compositions and methods for the treatment of cardiomyopathy. Several embodiments provided for herein relate to virally-mediated transfer of a gene to host cells to induce expression of an encoded polypeptide, protein or other product in order to ameliorate one or more symptoms of the cardiomyopathy in a subject. In several embodiments, the disclosed methods and compositions relate to recombinant adeno-associated virus particles encoding human RBM20 in order to treat cardiomyopathies, including dilated cardiomyopathy.

A recombinant adeno-associated virus (rAAV) comprising an AAV capsid and a vector genome comprising a frataxin gene is provided. Also provided is a composition containing an effective amount of rAAV to ameliorate symptoms of Freidreich's ataxia, including, e.g., reduction in progression towards neurocognitive decline and / or cardiomyopathy.

The present disclosure relates in part to gene replacement for the treatment of cardiomyopathy. In embodiments, the present invention provides compositions and methods of use for the treatment of ALPK3 cardiomyopathy. In embodiments, the present invention provides a composition comprising a nucleic acid encoding all or a portion of an ALPK3 protein.

The application discloses application of recombinant human USP13 protein in preparation of a drug for treating diabetic cardiomyopathy, and belongs to the technical field of biological medicines.The application first proves that the expression of USP13 in myocardial tissue and serum is significantly reduced under the condition of diabetic cardiomyopathy (DCM); the recombinant human USP13 protein can obviously reduce the level of myocardial cell active oxygen, reduce the expression of NLRP3 inflammasome and active Caspase3 protein in a DCM in-vitro model induced by high sugar / palmitic acid; in a DCM mouse model injected with the recombinant human USP13 protein through a tail vein, myocardial cell apoptosis is inhibited, and the expression of NLRP3 inflammasome and the synthesis of TNF-alpha in the heart of the animal are reduced.USP13 is a human protein, has no obvious toxic side effects, is high in safety, is small in immunological rejection in theory, provides a new effective drug for the clinical treatment of DCM, and has important clinical application value and industrialization prospect.

This invention pertains to the pharmaceutical field and relates to a class of substituted indene compounds and their uses. Specifically, this invention relates to compounds of formula (I), or stereoisomers, tautomers, nitrides, hydrates, solvates, metabolites, pharmaceutically acceptable salts, or prodrugs of compounds of formula (I). The compounds and pharmaceutical compositions thereof involved in this invention, as myosin inhibitors, can be used to prepare medicaments for the prevention or treatment of myosin-related diseases, and particularly for the treatment of hypertrophic cardiomyopathy.

This invention discloses an intelligent terminal and early warning method for home management of dilated cardiomyopathy (DCM) in children, integrating multi-parameter monitoring, belonging to the field of intelligent health management technology. The method includes the following steps: establishing an electromagnetic event timeline in the home health monitoring environment; synchronously collecting and correlating electrocardiogram (ECG), blood oxygen saturation, and body movement signals according to a unified time reference to form an intelligent early warning baseline and generate a time anchor. This invention achieves synchronous correlation between multi-source physiological signals and interference by establishing an electromagnetic event timeline and time anchor, and dynamically rearranges sampling time to maintain signal continuity. Through a rhythmic breathing-type time control table and a dynamic interference isolation mechanism, the sampling rhythm is inversely coordinated with electromagnetic events, effectively improving the stability and accuracy of heart rhythm analysis and achieving intelligent early warning for dilated cardiomyopathy in children.

The application discloses application of CO1-NU MT-lncRNA in preparation of an anti-diabetic cardiomyopathy drug, and a product and a preparation method thereof, and belongs to the field of biological medicines. The application provides application of CO1-NU MT-lncRNA in preparation of an anti-diabetic cardiomyopathy drug, wherein the CO1-NU MT-lncRNA is shown as SEQ ID NO. 1. Based on the application, the application further provides a recombinant expression vector, a transformant, an anti-diabetic cardiomyopathy drug based on the CO1-NU MT-lncRNA and a pharmaceutical use of the anti-diabetic cardiomyopathy drug, and provides a preparation method of the anti-diabetic cardiomyopathy drug. Animal tests prove that the anti-diabetic cardiomyopathy drug provided by the application can significantly improve the heart function of a diabetic cardiomyopathy animal, and plays an effective anti-diabetic cardiomyopathy role.

Providing quinazolindione compounds and their uses. [Solution] Quinazoline dione compounds are provided for treating cardiac indications such as hypertrophic cardiomyopathy and diastolic dysfunction. Diseases treated by the methods described herein include, but are not limited to, cardiomyopathy, hypertrophic cardiomyopathy (HCM), abnormal heart rhythms, aortic disease, Marfan syndrome, coronary artery disease, heart attack, heart failure, rheumatic heart disease, peripheral vascular disease, stroke, deep vein thrombosis, and pulmonary embolism.

The present invention relates to a compound of formula (I) as inhibitors of calcium calmodulin dependent protein kinase 2 (CAMK2) for the treatment of for the treatment of heart failure, fibrosis, cardiomyopathies, atrial fibrillation, catecholaminergic polymeric ventricular tachycardia, heart block, cardiac arrhythmias, contraception, anxiety, post-traumatic stress disorder, hypertension, tachycardia, diabetes, allergy, and asthma.

This invention discloses a novel copper death inhibitor and its application in the preparation of drugs for treating sepsis, belonging to the fields of pharmaceutical formulation and biomedicine. This invention discloses a method for preparing a novel copper death inhibitor, which can be used to develop highly efficient and low-toxicity copper death inhibitors. This agent can be used to prepare drugs for preventing sepsis-related organ damage and is a potential treatment for sepsis. It can inhibit copper death in sepsis-induced lung, kidney, liver, and cardiomyopathy, and reduce inflammatory responses and organ damage. Furthermore, this invention has the outstanding advantages of high specificity, high bioavailability, significant efficacy, and a stable preparation method, showing broad application prospects.

The present disclosure relates to the treatment and prevention of diseases and conditions (eg. cardiomyopathy) through LINC complex inhibition. A LINC complex inhibitor is provided for use in a method of treating or preventing a disease or condition characterised by microtubule dysfunction and / or a disease or condition characterised by sarcomere deficiency or dysfunction.

The present invention relates to a compound of formula (I) as inhibitors of calcium calmodulin dependent protein kinase 2 (CAMK2) for the treatment of for the treatment of heart failure, fibrosis, cardiomyopathies, atrial fibrillation, catecholaminergic polymeric ventricular tachycardia, heart block, cardiac arrhythmias, contraception, anxiety, post-traumatic stress disorder, hypertension, tachycardia, diabetes, allergy, and asthma.

This invention provides the use of a reagent overexpressing Parp7 in the preparation of drugs for treating septic cardiomyopathy, belonging to the field of biomedical technology. This invention involves constructing a recombinant adeno-associated virus vector AAV9-F4 / 80- that specifically overexpresses PARP7 on macrophages. Parp7 The drug was intravenously injected into mice, and a septic cardiomyopathy model was established using lipopolysaccharide induction. Experimental results showed that macrophage-specific overexpression of PARP7 significantly reduced serum levels of myocardial injury markers CK-MB and cTnT, improved cardiac function indicators such as ejection fraction and fractional shortening, alleviated myocardial tissue pathological damage, and inhibited macrophage infiltration and inflammatory factors. Ifn-beta , Tnf- α , Il‑6 and Il‑1β The expression of PARP7. This invention reveals the protective role of PARP7 in septic cardiomyopathy, providing a new target and strategy for the treatment of septic cardiomyopathy.