11 results about "Sodium current" patented technology

Fused heteroaryl compounds and compositions useful for preventing and / or treating a disease or condition related to aberrant function of voltage-gated sodium ion channels, e.g., an abnormal, delayed / persistent sodium current. Treatment methods for a disease or condition related to aberrant function of sodium ion channels are also provided herein, including neurological disorders (e.g., Dravet syndrome, epilepsy), pain, and neuromuscular disorders.

The present disclosure relates to non-racemic compositions of ranolazine and enantiomerically pure formulations and pharmaceutical compositions of ranolazine that are used in the treatment of diseases wherein the pathology of the disease includes a contribution from VGSC mediated late sodium currents, such as e.g., heart diseases and various types of metastatic cancers.

We provide condensed heteroaryl compounds and compositions useful for preventing and / or treating diseases or conditions associated with abnormal function of voltage-gated sodium ion channels, such as abnormal delayed / persistent sodium currents. [Solution] In one embodiment, a compound of formula (I) or a pharmaceutically acceptable salt thereof is provided. TIFF2026062794000384.tif2550 The invention also provides methods for treating diseases or conditions associated with abnormal function of sodium ion channels, including Dravet syndrome or epilepsy.

This invention discloses the application of the scorpion venom polypeptide BmK AS in the treatment of chronic epilepsy. BmK AS exerts potent anti-epileptic and neuroprotective effects through a confluence mechanism. In a lycine-induced mouse model, BmK AS significantly shortened seizure duration, reduced seizure frequency, prolonged seizure latency, and improved cognitive and mental outcomes. Electrophysiologically, BmK AS nonlinearly inhibited multiple VGSC subtypes, with a particularly significant effect on Nav1.6, reducing peak sodium current by 43% at a concentration of 5 nM. Furthermore, BmK AS alleviated hippocampal neuroinflammation by inhibiting the NLRP1 inflammasome pathway and related pyroptosis. This invention establishes BmK AS as a promising multi-mechanism therapeutic candidate, highlighting the value of a dual therapeutic strategy of Nav1.6 blockade and neuroinflammation suppression for epilepsy treatment.

The present invention is directed to, in part, fused heteroaryl compounds and compositions useful for preventing and / or treating a disease or condition relating to aberrant function of a voltage-gated, sodium ion channel, for example, abnormal late / persistent sodium current. Methods of treating a disease or condition relating to aberrant function of a sodium ion channel including neurological disorders (e.g., Dravet syndrome, epilepsy), pain, and neuromuscular disorders are also provided herein.

The present invention is directed to, in part, compositions or dosage forms comprising fused heteroaryl compounds useful for preventing and / or treating a disease or condition relating to aberrant function of a voltage-gated, sodium ion channel, for example, abnormal late / persistent sodium current. Methods of treating a disease or condition relating to aberrant function of a sodium ion channel including neurological disorders (e.g., Dravet syndrome, epilepsy), pain, neuromuscular disorders, trigeminal autonomic cephalalgia (TAC), migraine, cranial neuropathy or multiple cranial neuropathy, and cortical spreading depression (CSD)are also provided herein. In another aspect, the present invention provides a method of making ion channel modulators.

We provide formulations of ion channel modulators. [Solution] The present invention partially relates to compositions or dosage forms comprising condensed heteroaryl compounds useful for preventing and / or treating diseases or conditions associated with abnormal function of voltage-gated sodium ion channels, such as abnormal delayed / persistent sodium currents. Methods for treating diseases or conditions associated with abnormal function of sodium ion channels, including neurological disorders (e.g., Dravet syndrome, epilepsy), pain, neuromuscular disorders, trigeminal-autonomic headache (TAC), migraines, cranial nerve disorders or polycranial nerve disorders, and cortical spreading depression (CSD), are also provided herein. In another aspect, the present invention provides methods for producing ion channel modulators.

The present invention is directed to, in part, fused heteroaryl compounds and compositions useful for preventing and / or treating a disease or condition relating to aberrant function of a voltage-gated, sodium ion channel, for example, abnormal late / persistent sodium current. Methods of treating a disease or condition relating to aberrant function of a sodium ion channel including neurological disorders (e.g., Dravet syndrome, epilepsy), pain, and neuromuscular disorders are also provided herein.

The invention relates to application of an OGN overexpression vector in preparation of a medicine for preventing reperfusion arrhythmia, and belongs to the technical field of medicines. In order to solve the problem that an existing anti-arrhythmia drug cannot effectively prevent reperfusion arrhythmia, the invention provides application of an OGN overexpression vector in preparation of a drug for preventing reperfusion arrhythmia, and the OGN overexpression vector is a recombinant adeno-associated virus vector and contains a nucleotide sequence for coding OGN. According to the invention, the recombinant adeno-associated virus vector carrying the OGN gene is constructed to drive the efficient expression of the OGN gene in myocardial cells, and the Nav1.5 protein expression level is up-regulated and the sodium current peak value is increased, so that the normal rhythm of cardiac electrophysiological activity is maintained, and the targeted improvement of the sodium ion channel function of the myocardial cells and the stability of cardiac electrical conduction are realized. The time window design of the preventive drug is highly matched with the clinical diagnosis and treatment process, and the preventive drug has extremely high operability and clinical transformation potential.

A method of increasing sodium current in a cardiac cell generally includes introducing into the cardiac cell an miR-448 inhibitor in an amount effective to decrease miR-448 suppression of SCN5A mRNA transcription, thereby increasing sodium current in the cardiac cell. A method of increasing translation of SCN5A mRNA in a cell generally includes introducing into the cell an miR-448 inhibitor in an amount effective to decrease miR-448 suppression of SCN5A mRNA transcription. A method of decreasing arrythmia in a cardiac cell generally includes introducing into the cardiac cell an miR-448 inhibitor in an amount effective to decrease miR-448 suppression of SCN5A mRNA transcription. A method of treating arrythmia in a patient having, or at risk of having, arrythmia generally includes administering to the patient an miR-448 inhibitor in an amount effective to decrease the likelihood or extent of arrythmia in the patient. In some embodiments of all methods, the miR-448 inhibitor can be an miR-448 antagomir or an miR-448 sponge.

The application relates to application of an OGN overexpression vector in preparation of a reperfusion arrhythmia prevention drug and belongs to the technical field of medicines. In order to solve the problem that the existing anti-arrhythmia drugs cannot effectively prevent reperfusion arrhythmia, the application provides application of an OGN overexpression vector in preparation of a reperfusion arrhythmia prevention drug, the OGN overexpression vector is a recombinant adeno-associated virus vector, and the OGN overexpression vector contains a nucleotide sequence coding OGN. The application constructs a recombinant adeno-associated virus vector carrying an OGN gene, drives efficient expression of the OGN gene in myocardial cells, up-regulates the expression level of Nav1.5 protein, increases the peak value of sodium current, thereby maintaining the normal rhythm of cardiac electrophysiological activity, and realizes targeted improvement of the function of the sodium ion channel of the myocardial cells and the stability of the cardiac electrical conduction. The time window design of the prevention drug of the application is highly consistent with the clinical diagnosis and treatment process, and the prevention drug has strong operability and clinical transformation potential.