30 results about "Sodium current" patented technology

The present invention provides methods of treating neurological disorders in a mammal by administering to the mammal an effective amount of a selective persistent sodium channel antagonist that has at least 20-fold selectivity for persistent sodium current relative to transient sodium current.

The invention provides short interfering nucleic acids, either single-stranded or double-stranded, that cause RNAi-induced degradation of mRNA from the Nav1.8 sodium channel gene; to pharmaceutical compositions comprising such short interfering nucleic acids; recombinant vectors comprising such short interfering nucleic acids; a method for inhibiting translation of an mRNA; a method for inhibiting expression of a polypeptide; a method for blocking the membrane potential in a cell; a method for blocking the sodium current in a cell; and a method for inhibiting chronic pain.

The present invention provides methods of treating chronic pain in a mammal by administering to the mammal an effective amount of a selective persistent sodium channel antagonist that has at least 20-fold selectivity for persistent sodium current relative to transient sodium current.

The invention relates to a mechanical arm movement rhythm control method based on a CPG neural network. The method comprises the following steps that (1) an upper computer is used for setting electricconductivity and reverse potential parameters corresponding to nerve cell continuous sodium current, potassium current and leakage current as well as an upper limit threshold value, a lower limit threshold value and a threshold value period during variable-threshold shaping, and transmitting the electric conductivity, the reverse potential parameters, the upper limit threshold value, the lower limit threshold value and the threshold value period to the FPGA through USB communication; (2) the FPGA is used for establishing a CPG neural network simulation model according to the set parameters, simulation is carried out, a discharge waveform is output in the simulation process, and the waveform is transmitted to the upper computer to be displayed; (3) the FPGA is used for achieving variable-threshold shaping, the discharge waveform output by the CPG neural network in the step 2 is set, moreover, a control signal is output to a mechanical arm so as to control and adjust the movement rhythmof the mechanical arm, and the angular displacement of a mechanical arm joint is transmitted to the upper computer to be displayed.

The present application discloses a method of slowing inactivation of sodium current in a cell by contacting the cell with dimethyl lithospermate B.

The invention provides a preparation method of Korean mondshood root total alkaloids and applications in preparing a slow sodium-ion passage blocking agent and preparing drugs for resisting arrhythmia. Both the Korean mondshood root total alkaloids and the guanfu base I are provided to have an effect for inhibiting slow sodium current of ventricular muscles of cavies. The invention particularly relates to an application of guanfu base VIIII in preparing a drug-metabolizing enzyme inhibitor. The invention also provides an application of guanfu base VIIII in preparing a slow sodium-ion passage blocking agent.

The invention discloses a novel application of a traditional Chinese medicine extract product-Arctigenin in preparation of anti-arrhythmia medicines. A research found that the Arctigenin has bidirectional anti-arrhythmia effect and can adjust arrhythmia caused by aconitine and ouabain. Arctigenin has an effect for reducing ventricular muscle contraction force. A pharmacological effect of the Arctigenin is bidirectional adjusted cardiac muscle cell inner calcium current, the cardiac muscle cell inner potassium current is increased, and the sodium current is inhibited. The invention shows that the Arctigenin has anti-arrhythmia effect, and especially has bidirectional adjusting on arrhythmia, the side-effect is smaller, the Arctigenin has application prospect for treating toxic arrhythmia and ischemic-reperfusion arrhythmia in aconitine and ouabain; and the Arctigenin with myocardial contractility reduction effect can be taken as an auxiliary treatment measurement for hypertensive disease.

The invention discloses application of an adrenergic receptor antagonist in preparation of a drug for relieving sodium current increasing caused by brain injury. After a hypoxic-ischemic brain injury mouse is injected with the adrenergic receptor antagonist, the change of a sodium channel and increasing of a current amplitude can be significantly relieved, so that the adrenergic receptor antagonist can be applied to the preparation of the drug for relieving the sodium current increasing caused by the brain injury and has a potential application prospect in the treatment field of the brain injury.

The present invention relates to a method for slowing the development of mammalian organ, tissue and cellular damage and death by using a persistent sodium current blocker (or a pharmaceutically acceptable salt or derivative thereof). The present invention further relates to a method for preventing damage and death in mammalian organs, tissues and cells or reducing the extent of damage and death in mammalian organs, tissues and cells. In particular the invention relates to a method for the treatment, amelioration or prevention of non-neuronal and non-myocardial cell or tissue damage or death and for reducing the pain associated with non-neuronal and non-myocardial cell or tissue damage.

The present invention is directed to methods of treating diseases or conditions mediated by elevated persistent sodium channel, such as ocular disorders, pain, multiple sclerosis, and seizure disorders utilizing a compound of Formula Ior a pharmaceutically acceptable salt thereof or a pharmaceutical composition comprising said compound, wherein variables R, R1, R2, R3, R4, R5, m, and n in Formula I are as defined herein.

The invention relates to a novel South China Sea conus littertus Linnaeus P-superfamily toxin polypeptide sequence 1t9b with post-translational modification, and an application of the polypeptide to the neurobiological study, ionic channel study and analgesic development. The invention obtains the 1t9b from the toxic pipe of the South China Sea signal conus through a plurality of separation and purification methods, and the amino acid sequence of the 1t9b is showed by the andlt;400andgt;1 sequence in a sequence table. The conus toxin 1t9b has an obvious inhibiting action on a TTX sensitive type sodium current in a density of 500nM. A mouse hot plate experiment also discloses that the conus toxin 1t9b has a central analgesia action. Thus, the conus toxin 1t9b can serve as a probe which is applicable to the classification and determination of ion channel types and hypotypes or to the research and development of instrumental medicines and the preparation of analgesics.

The invention provides a preparation method of total alkaloids of radix aconiti coreani as well as an application of the total alkaloids of radix aconiti coreani in preparing a slow sodium ion channel blocker and an antiarrhythmic medicine. Researches show that both the total alkaloids of radix aconiti coreani and Guanfu A hydrochlorate have an inhibiting effect on a slow sodium current of the ventricular muscle of a guinea pig. The invention particularly relates to an application of the Guanfu base I in preparing enzyme inhibitors for drug metabolism. The invention further provides an application of the Guanfu base A in preparing the slow sodium ion channel blocker.

The invention provides application of sodium houttuyfonate to preparation of a medicament for treating heart failure and / or arrhythmia. The invention also provides application of the sodium houttuyfonate to preparation of a medicament for enhancing contractile force of ventricular myocytes. The sodium houttuyfonate increases L-type calcium current (Ica.L), and can improve myocardial systolic dysfunction caused by the reduction of sarcoplasmic reticulum Ca release when the heart failure is occurred. The sodium houttuyfonate blocks peak sodium current (Ina.p) and has the characteristics of class-I antiarrhythmic medicaments, and can also block late sodium current (INa.L) increased by the induction of congestin II (ATX-II) and has the potential of inhibiting the arrhythmia caused by the increment of the INa.L.

The invention provides a preparation method of Korean mondshood root total alkaloids and applications in preparing a slow sodium-ion passage blocking agent and preparing drugs for resisting arrhythmia. Both the Korean mondshood root total alkaloids and the guanfu base I are provided to have an effect for inhibiting slow sodium current of ventricular muscles of cavies. The invention particularly relates to an application of guanfu base VIIII in preparing a drug-metabolizing enzyme inhibitor. The invention also provides an application of guanfu base VIIII in preparing a slow sodium-ion passage blocking agent.

The present invention is directed to a compound of Formula Ior a pharmaceutically acceptable salt thereof; wherein R, R1, R2, R3, R4, m, and n are as defined herein, to pharmaceutical compositions comprising said compound, and to methods of treating diseases or conditions mediated by elevated persistent sodium current, such as an ocular disorder, multiple sclerosis, seizure disorder, and chronic pain.

The invention provides short interfering nucleic acids, either single-stranded or double-stranded, that cause RNAi-induced degradation of mRNA from the Nav1.8 sodium channel gene; to pharmaceutical compositions comprising such short interfering nucleic acids; recombinant vectors comprising such short interfering nucleic acids; a method for inhibiting translation of an mRNA; a method for inhibiting expression of a polypeptide; a method for blocking the membrane potential in a cell; a method for blocking the sodium current in a cell; and a method for inhibiting chronic pain.

The invention belongs to the technical field of icariin applications, and discloses applications of icariin in preparation of medicines treating arrhythmia. According to a technical scheme, the medicines are capsules, micro-capsules, lipidosomes, granules, injections, tablets or oral liquids. Beneficial effects of the applications are that the icariin can prolong occurrence time (a time threshold) and increase the using amount (a dosage threshold) for arrhythmia induced by aconitine under a whole (living body) condition, and the icariin can effectively reduce the occurrence rates of ventricular tachycardia and ventricular fibrillation which are induced by the aconitine and the death rate of New Zealand big-ear rabbits. The icariin can retard instantaneous sodium current (I<NaT>), late sodium current (I<NaL>) and L-type calcium current (I<CaL>) and plays a role of an arrhythmia preventing medicine. The icariin has no obvious effects on inward rectifier potassium current (I<K1>) of left-ventricular muscle (LVM), rapid delayed rectifier potassium current (I<Kr>), instantaneous outward potassium current (I<to>) of left atrial muscle (LAM) and ultra-rapidly activated delayed rectifier potassium current (I<Kur>), thus improving medication safety.

The invention relates to application of a 3-phenylfuran substituted 2-phenyl-4H-benzo[1,3]oxazine derivative. The invention provides a sodion channel blocker. The sodion channel blocker is a 3-phenylfuran substituted 2-phenyl-4H-benzo[1,3]oxazine derivative. The compound can effectively inhibit a sodion channel and reduce sodium current, and has the potential of treating neuropathic pain, such as post-herpes zoster neuralgia, diabetic neuralgia, trigeminal neuralgia, spinal cord injury and the like.

A 26 residue peptide (Am2766) with the sequence CKQAGESCDIFSQNCCVGTCAFICIE-NH2 has been isolated and purified from the venom of the molluscivorous snail, Conus amadis, collected of the southeastern coast of India. Chemical modification and mass spectrometric studies establish that Am2766 has three disulfide bridges. Cterminal amidation has been demonstrated by mass measurements on the C-terminal fragments obtained by proteolysis. Sequence alignments establish that Am2766 belongs to the δ-conotoxin family. Am2766 inhibits the decay of the sodium current in brain rNav1.2a voltage-gated Na+ channel, stably expressed in Chinese hamster ovary (CHO) cells. Unlike δ-conotoxins have previously been isolated from molluscivorous snails, Am 2766 inhibits inactivation of mammalian sodium channel.