Sodium channel protein type 9 subunit alpha

Description:

Description
  • Accession: Q15858
  • Swissprot: SCN9A_HUMAN
  • Organism: Homo sapiens
  • Gene: SCN9A
  • Target class: Ion channel

Drug Relations:

benzocaine
A surface anesthetic that acts by preventing transmission of impulses along NERVE FIBERS and at NERVE ENDINGS. Bioactivity details MOA
carbamazepine
A dibenzazepine that acts as a sodium channel blocker. It is used as an anticonvulsant for the treatment of grand mal and psychomotor or focal SEIZURES. It may also be used in the management of BIPOLAR DISORDER, and has analgesic properties. Bioactivity details MOA
eslicarbazepine acetate
Eslicarbazepine acetate is extensively converted to eslicarbazepine, which is considered to be responsible for therapeutic effects in humans. The precise mechanism(s) by which eslicarbazepine exerts anticonvulsant activity is unknown but is thought to involve inhibition of voltage-gated sodium channels. Bioactivity details MOA
ethotoin
Ethotoin exerts an antiepileptic effect without causing general central nervous system depression. The mechanism of action is probably very similar to that of phenytoin. The latter drug appears to stabilize rather than to raise the normal seizure threshold, and to prevent the spread of seizure activity rather than to abolish the primary focus of seizure discharges. Bioactivity details MOA
lacosamide
a functionalized amino acid, selectively enhances slow inactivation of voltage-gated sodium channels, resulting in stabilization of hyperexcitable neuronal membranes and inhibition of repetitive neuronal firing, indicated for partial-onset seizures Bioactivity details MOA
lamotrigine
A phenyltriazine compound, sodium and calcium channel blocker that is used for the treatment of SEIZURES and BIPOLAR DISORDER. Bioactivity details MOA
lidocaine
A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE. Bioactivity details MOA
mephenytoin
An anticonvulsant effective in tonic-clonic epilepsy (EPILEPSY, TONIC-CLONIC). It may cause blood dyscrasias. Bioactivity details MOA
mepivacaine
A local anesthetic that is chemically related to BUPIVACAINE but pharmacologically related to LIDOCAINE. It is indicated for infiltration, nerve block, and epidural anesthesia. Mepivacaine is effective topically only in large doses and therefore should not be used by this route. (From AMA Drug Evaluations, 1994, p168) Bioactivity details MOA
mexiletine
Antiarrhythmic agent pharmacologically similar to LIDOCAINE. It may have some anticonvulsant properties. Bioactivity details MOA
orphenadrine
A muscarinic antagonist used to treat drug-induced parkinsonism and to relieve pain from muscle spasm. Bioactivity details MOA
phenazopyridine
A local anesthetic that has been used in urinary tract disorders. Its use is limited by problems with toxicity (primarily blood disorders) and potential carcinogenicity. Bioactivity details MOA
phenytoin
An anticonvulsant that is used to treat a wide variety of seizures. It is also an anti-arrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant effect appears to involve a reduction in the sensitivity of muscle spindles to stretch. Phenytoin has been proposed for several other therapeutic uses, but its use has been limited by its many adverse effects and interactions with other drugs. Bioactivity details MOA
procainamide
A class Ia antiarrhythmic drug that is structurally-related to PROCAINE. Bioactivity details MOA
ropivacaine
An anilide used as a long-acting local anesthetic. It has a differential blocking effect on sensory and motor neurons. Bioactivity details MOA
rufinamide
The precise mechanism(s) by which rufinamide exerts its antiepileptic effect is unknown. The results of in vitro studies suggest that the principal mechanism of action of rufinamide is modulation of the activity of sodium channels and, in particular, prolongation of the inactive state of the channel. Bioactivity details MOA
tetracaine
Local ester anesthetic that blocks both the initiation and conduction of nerve impulses by decreasing the neuronal membrane's permeability to sodium ions, which results in inhibition of depolarization with resultant blockade of conduction. Bioactivity details MOA
tocainide
An antiarrhythmic agent which exerts a potential- and frequency-dependent block of SODIUM CHANNELS. Bioactivity details MOA
amitriptyline
Tricyclic antidepressant with anticholinergic and sedative properties. It appears to prevent the re-uptake of norepinephrine and serotonin at nerve terminals, thus potentiating the action of these neurotransmitters. Amitriptyline also appears to antagonize cholinergic and alpha-1 adrenergic responses to bioactive amines. Bioactivity details MOA
safinamide
Safinamide acts through both dopaminergic and non-dopaminergic mechanisms of action. Safinamide is a highly selective and reversible MAO-B inhibitor causing an increase in extracellular levels of dopamine in the striatum. Safinamide is associated with state-dependent inhibition of voltage-gated sodium (Na+) channels, and modulation of stimulated release of glutamate. To what extent the nondopaminergic effects contribute to the overall effect has not been established. Bioactivity details MOA