169 results about "Cardiotoxicity" patented technology

Methods, systems and circuits predict cardiotoxicity induced cardiac injury prior to an irreversible state by electronically generating at least one histogram of mean intensities of voxels / pixels in an MRI image of a left ventricle myocardium and electronically determining a likelihood of cardiac injury due to cardiotoxicity based on data from the at least one histogram.

Methods, systems and circuits predict cardiotoxicity induced cardiac injury prior to an irreversible state by electronically generating at least one histogram of mean intensities of voxels / pixels in an MRI image of a left ventricle myocardium and electronically determining a likelihood of cardiac injury due to cardiotoxicity based on data from the at least one histogram.

Devices and methods for performing extracellular recording of cells, such as excitable cells, cardiomyocytes, and cardiomyocyte precursor cells is provided. An exemplary device includes a nonconductive substrate forming or provided as a base of one or more wells; a recording electrode positioned on the substrate within the well, wherein the recording electrode is accessible to cells when a cell sample is added to the device; and a reference electrode positioned within the well in a cell-free zone, the cell-free zone characterized as free from contact with cells when the cell sample is added to the device, thereby preventing contact between cells and the reference electrode.

Disclosed are assays, methods, and kits for the screening of test compounds for their capability to induce cardiotoxicity in a subject. In particular, whether a test compound has the effect to prolong the Q-T interval as measured by an electrocardiogram in a human. The assays, methods, and kits disclosed herein make use of the binding interaction between novel fluorescent tracers and the hERG K+ channel, and the propensity of a test compound to influence that binding interaction.

Novel iron chelators exhibiting neuroprotective and good transport properties are useful in iron chelation therapy for treatment of a disease, disorder or condition associated with iron overload and oxidative stress, eg. a neurodegenerative or cerebrovascular disease or disorder, a neoplastic disease, hemochromatosis, thalassemia, a cardiovascular disease, diabetes, a inflammatory disorder, anthracycline cardiotoxicity, a viral infection, a protozoal infection, a yeast infection, retarding ageing, and prevention and / or treatment of skin ageing and skin protection against sunlight and / or UV light. The iron chelator function is provided by a 8-hydroxyquinoline, a hydroxypyridinone or a hydroxamate moiety, the neuroprotective function is imparted to the compound e.g. by a neuroprotective peptide, and a combined antiapoptotic and neuroprotective function by a propargyl group.

The invention provides a composition with anti-tumor effect and application thereof. The composition consists of 0.01 to 10 weight parts of pure bufadienolide compound, extract rich in bufadienolide compound, raw toad venom or toad skin and 0.01 to 99.9 weight parts of medicament with anti-arrhythmic effect. The composition with the anti-tumor effect has the advantage that the match among the components is scientific and reasonable; multiple in vitro tumor cytotoxicity and in vivo tumor inhibiting experiments show that the composition provided by the invention has good anti-tumor effect and plays a role in synergy after combination; and cardiotoxic experiments show that the cardiotoxicity of the composition provided by the invention is obviously reduced, and the composition can reduce the cardiotoxicity caused by primary single use of the bufadienolide compound, the toad venom or the toad skin and plays a role in detoxifying. Therefore, the composition is safer and more effective to use, and is expected to develop a new generation anti-cancer medicament.

The present invention provides a method, system and composition for screening drug candidates for cardiotoxicity and for novel drugs that effect cardiomyocyte contractility and function. The invention provides an efficient and reliable screening assay to detect the effect of new and potential drug candidates on cardiomyocyte calcium flux, membrane depolarization, and / or the propagation of action potentials.

The present invention relates generally to the prevention and / or treatment of cardiac and stroke injury. In particular, the present invention provides compositions and methods for preventing and treating tissue injury in cardiac and stroke settings and injury due to ischemia / reperfusion, hypoxia, cardiotoxicity of certain therapeutic regimens, and other causes, by administering an agent that inhibits sphingosine-1-phosphate lyase (SPL) activity.

The invention relates to a drug for prevention and treatment of cardiotoxicity induced by anthracycline antibiotics, and an application thereof. Flavone can be adopted for preparing the drug for prevention and treatment of the cardiotoxicity induced by the anthracycline drugs after modifying a plurality of sites such as 3, 5, 6, 7, 3', 4' and the like on the chemical structural formula of the flavone. The experimental results show that: with the flavone compounds, the cardiotoxicity induced by adriamycin can be reduced, myocardial contraction function can be improved, and oxygen radicals can be removed; cardiac tissue overoxidation damage induced by the adriamycin can be reduced, and cardiac function can be improved; the cardiotoxicity to the human body induced by the anthracycline drugs during chemotherapy can be effectively reduced, the pain of the patient undergoing the chemotherapy can be reduced, and the death rate caused by the anthracycline drugs can be reduced.

The disclosure relates to methods of ameliorating or preventing cardiotoxicity caused by anti-neoplastic agents, such as doxorubicin, by administering to a patient oxypurinol, salt or derivatives thereof, before, during or after administration of the anti-neoplastic agent.

The invention discloses a drug cardiotoxicity detection analysis method based on a myocardial cell sensor. According to the drug cardiotoxicity detection analysis method, a high-performance and low-cost cardiac muscle cell sensor is constructed by adopting ex vivo myocardial cell culture; the change of pulsation images when myocardial cells mechanically pulsate is calculated and detected by adopting algorithms such as image acquisition, conversion of an RGB image into a gray level image, image binaryzation, image matrixing and peak detection, and the mechanical pulsation of the myocardial cells is quantized by using a difference value of the pulsation images, the detection on a rate, an amplitude and a pulsation interval of mechanical pulsation of the myocardial cells is realized; by analyzing the change of the mechanical pulsation state of the myocardial cells over time under the drug action, the cardiotoxicity of a drug is evaluated. Compared with an existing drug cardiotoxicity detection analysis method, the drug cardiotoxicity detection analysis method has the advantages of no marks, no loss, low cost, simple operating steps, and the like, and is capable of observing and evaluating the drug cardiotoxicity simply for a long time.

The invention relates to a method for screening anthracycline cardiotoxicity genes through mRNA expression profiles and competitive endogenesis RNA expression profiles jointly. The method includes the steps that expression values of a large quantity of genes are detected through mRNA and competitive endogenesis RNA expression profile chips, and the correlations of all the genes are ordered; the obtained mRNA feature genes and the obtained competitive endogenesis RNA feature genes are combined; a gene pool is subjected to further gene selection with a genetic algorithm; differential expression genes are selected by comparing the data between different samples of mRNA and competitive endogenesis RNA joint expression profiles of breast cancer patients, breast cancer AIC patients and able-bodied persons; the differential expression genes are predicted, and the genes with the scores larger than 140 and free energy smaller than 20 are selected as reliable target genes; genes with obvious differences are selected from the target genes, and constructed breast-cancer anthracycline cardiotoxicity attacking target genes are verified through the residual RNA. By means of the method, more reliable potential gene markers related to anthracycline cardiotoxicity can be selected as a candidate.

The present invention relates to therapeutic uses of ErbB ligands, including betacellulin. The therapeutic uses include methods of using ErbB ligand family compounds alone, or in conjunction with other agents, for reducing blood glucose levels, treating Type I and Type II diabetes, obesity, muscle wasting diseases, and cardiotoxicity.

The present invention provides lipid emulsions and methods of intravenously administering lipid emulsions to treat systemic toxicity caused by foreign lipophilic and amphiphilic substances. In particular, methods are provided to treat cardiovascular impairment, such as cardiotoxicity, asystole and ischemia of the brain and heart, and neurological impairments, such as seizures and comas, caused by foreign lipophilic and amphiphilic substances, including cardiovascular impairment caused by local anesthetics, tricyclic antidepressants, sodium channel blockers, and calcium channel blockers.

The invention discloses a micro-molecule fluorescent probe of a phenyl furan hERG potassium channel and application thereof. The structure general formula of the fluorescent probe is as shown in a formula (I), wherein R1 is a single substituted group or a polysubstituted group of halogen, alkyl or alkoxy; R2 is fluorophore; n is 1-6; the piperazine ring and the fluorophore are connected by an alkyl chaing containing 1-6 carbons. The molecule of the fluorescent probe can be used for marking an hERG potassium channel, can be used for screening activity of an hERG potassium channel inhibitor and evaluating the cardiotoxicity of commercial medicines, or used as a tool drug for pharmacological, pathological and physiological researches related to hERG potassium channels. Furthermore, the preparation method of the compound is mild in reacting condition, the raw materials have low price and are easily available, and the operation and posttreatment are simple.

This disclosure provides methods and pharmaceutical compositions for reducing or eliminating cardiotoxicity, particularly cardiotoxicity induced by a cancer treatment or other therapy. In some cases, the methods and compositions prevent or reduce cardiotoxicity caused by anthracycline treatment. The methods provided herein often comprise administering a protective agent such as myricetin, tricetin, robinetin, ficetin, vitexin, quercetin, dihydrorobinetin, kaempferol, 7,3′,4′,5′-tetrahydroxyflavone, and myricitrin in conjunction with the administration of a cancer drug or other treatment. They may comprise administering a protective agent in combination with dexrazoxane. The compositions provided herein include co-formulations of a protective agent with a different protective agent or with a cancer treatment (e.g., anthracycline drug).

The present invention relates to the use of cardiac hormones, particularly natriuretic peptides, for diagnosing the risk of suffering from a cardiovascular complication, particularly heart disease or acute coronary syndrome, as a consequence of cardiotoxic medication, in particular chemotherapeutics, including anthracyclines. In particular, the invention relates to a method for diagnosing the risk of a patient who is going to receive cardiotoxic medication of suffering from a cardiovascular complication as a consequence of the cardiotoxic medication, comprising the steps of (a) taking a body fluid or tissue sample, and (b) measuring, preferably in vitro, the level of a cardiac hormone. Preferred cardiac hormones in the context of the present invention are ANP, NT-proANP, BNP, and NT-proBNP.

The present invention provides a method of determining toxicity to the heart of an anthracycline-type anticancer chemotherapeutic agent such as adriamycin etc., which comprises detecting human H-FABP (Human Heart-type Fatty Acid-Binding Protein) in the blood separated from human, a reagent therefor, a kit therefor and the like.

The invention belongs to the field of medicine, which relates to Deferiprone and a novel medicated purpose of a Deferiprone preparation, in particular to Deferiprone (1,2- dimethyl-3-hydroxide radical-4-pyridine, Deferiprone) and the application of the Deferiprone preparation in the prevention and curing of Anthracycline medicine heart toxicity. The invention researches the preventing and curing function of the Deferiprone to bandicoot heart toxicity caused by Adriamycin from the cell level, the tissue level and the whole level and prepares biodegradable type Deferiprone implant, Deferiprone troche, capsule, oral liquor and injection that can release medicine continuously. An experimental result proves that the Deferiprone and the Deferiprone preparation can not only improves the cardiac muscle shrinkage functions and protects the myocardial cell organ structure, but also complexes free iron ions directly, reduces the heart toxicity and other side and toxic effects caused by the Anthracycline medicine obviously and the mortality rate caused by the Anthracycline medicine.

The likelihood that a compound will exhibit cardiotoxicity in an in vitro or in vivo assay predicted by the ability of the compound to inhibit at least one kinase from a selected group.

The invention provides a method for establishing a micro-fluidic chip based human heart model. A micro-fluidic chip mainly comprises a cell inlet pool, channels, a cell culture chamber and an outlet pool, wherein the cell culture chamber is connected to the cell inlet pool and the cell outlet pool through straight channels; and the cell culture chamber has a structure having repeated hexagonal bulges. The method for establishing a human heart model comprises the following steps: (1) directionally differentiating hiPSC into myocardial cells; (2) modifying the chip; (3) inoculating and culturing cells in the chip; and (4) establishing the human heart model. The model is used for observing representations of cell activity investigation and function changes in the chip, and can be used for human heart auxology researches and drug cardiotoxicity. The micro-fluidic chip based human heart model is used for observing morphologic changes and arrangement of myocardial cells having a micro-structural surface under the perfusion condition at different flow-speeds, especially for the influence of blood flow shearing force and matrix surface microstructure on the myocardial cell developmental maturity in the heart developing process.

The present invention relates to matriptase antibodies and immunoconjugates of matriptase antibodies with cytotoxic agents and the use thereof for killing or inhibiting the growth of matriptase-expressing cancer cells, such as those of multiple myeloma and breast cancers. In particular, immunoconjugates comprising a matriptase monoclonal antibody and anticancer agents such as doxorubicin (DOX) are introduced, which are equipotent to anticancer agents used in free form but exhibit significantly reduced cardiotoxicity and almost no adverse effects on normal bone marrow-derived mesenchymal stromal cells that do not express matriptase. The present invention also provides compositions comprising these new immunoconjugates and use of them for treatment of malignancies comprising cells that express matriptase. In addition, administration of a matriptase antibody or immunoconjugates of a matriptase antibody and a cytotoxic agent in combination with administration of an immunomodulatory agent, such as thalidomide or an analog thereof, provides a more effective treatment of these cancers.

The present invention relates to methods of reducing cardiotoxicity and / or improving survival from treatment with anthracycline agents comprising administering a therapeutically effective amount of a composition comprising a vasopressin antagonist compound or a pharmaceutically acceptable salt thereof as an active ingredient, administered simultaneously or prior to the anthracycline administration.

Systems for assaying human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are provided. Aspects of the systems include a traction force microscopy substrate, such as a traction force microscopy hydrogel (TFM-hydrogel), having an adhesion protein domain on a surface thereof; a video imager configured to obtain video data from an hiPSC-CM present on the adhesion protein domain; and a processing module configured to receive the video data and derive a parameter of the hiPSC-CM therefrom. Also provided are methods of using the systems.

The present invention relates to lipoid microspere injection composition containing liposoluble toad cake extract and its preparation process. The injection composition contains liposoluble toad cake extract 0.0001-5 wt%, liposoluble medium 1-30 wt%, surfactant 0.5-10 wt%, isoosmotic regulator 0.5-10 wt%, and water for the rest. The injection has anticancer and analgetic effects, less blood vessel irritation caused by toad cake, no toxicity on heart and capacity of raising the medicine concentration inside tumor.

Methods for the treatment of HER2-positive breast cancer are provided by neoadjuvant administration of pertuzumab and trastuzumab in combination with anthracycline-based chemotherapy. In particular, the methods concerns the treatment patients with HER2-positive, locally advanced, inflammatory, or early-stage breast cancer by neoadjuvant administration of pertuzumab and trastuzumab following anthracycline-based chemotherapy, wherein the combined administration of pertuzumab and trastuzumab increases pathological complete response (pCR) relative to administration of trastuzumab as a single agent, without significant increase in adverse events, such as cardiac toxicity, relative to neoadjuvant anthracycline-based chemotherapy.

The invention belongs to the field of the genetic engineering, and particularly provides a group of DNA methylation biomarkers for evaluating cardiac muscle cell damage and an application thereof. TheDNA methylation biomarker comprises 30 DNA methylation sites of 5 DMRs corresponding to 5 cardiac muscle differentiation key factors; and the five cardiac muscle differentiation key factors are GATA4, TNNT2, TNNI3, MEF2A and NKX2-5. Such type of the provided differential DNA methylation biomarkers is successfully developed to subvert the traditional biomarkers using protein as major means, a newsituation is created for the prevention and treatment of the cardiac muscle damage, and a reference is provided for the development of other disease biomarkers. The DNA methylation biomarkers are capable of evaluating the damage level of the cardiac muscle affected by environmental factors, and evaluating and forecasting the cardiotoxicity of environmental chemistry, and are the biomarkers with the prospect.