Riluzole (CAS: 1744-22-5)
Background Information of Riluzole
Riluzole is a glutamate antagonist used as an anticonvulsant and to prolong the survival of patients with amyotrophic lateral sclerosis.
Target: Sodium Channel
Riluzole inhibits the release of glutamic acid from cultured neurons, and from brain slices.
Storage Condition of Riluzole
Quality Control and Spectral Data
Mechanism and Indications
||Sponsor & Collaborators
||2-Amino-6-(trifluoromethoxy)benzothiazole; 6-Trifluoromethoxy-2-aminobenzothiazole; 6-(Trifluoromethoxy)-1,3-benzothiazol-2-amine; 6-(trifluoromethoxy)benzo[d]thiazol-2-amine
Structure Information of Riluzole
Other Form Products of Riluzole
Recommended Products in Same Target
Recommended Products in the Same Indication
Chemical and Physical Properties
|Appearance:Light yellow to yellow Solid
.Doble, A., The pharmacology and mechanism of action of riluzole. Neurology, 1996. 47(6 Suppl 4): p. S233-41.
The excitotoxic hypothesis of neurodegeneration has stimulated much interest in the possibility of using compounds that will block excitotoxic processes to treat neurologic disorders. Riluzole is a neuroprotective drug that blocks glutamatergic neurotransmission in the CNS. Riluzole inhibits the release of glutamic acid from cultured neurons, from brain slices, and from corticostriatal neurons in vivo. It is thought these effects may be partly due to inactivation of voltage-dependent sodium channels on glutamatergic nerve terminals, as well as activation of a G-protein-dependent signal transduction process. Riluzole also blocks some of the postsynaptic effects of glutamic acid by noncompetitive blockade of N-methyl-D-aspartate (NMDA) receptors. In vivo, riluzole has neuroprotective, anticonvulsant, and sedative properties. In a rodent model of transient global cerebral ischemia, a complete suppression of the ischemia-evoked surge in glutamic acid release has been observed. In vitro, riluzole protects cultured neurons from anoxic damage, from the toxic effects of glutamic-acid-uptake inhibitors, and from the toxic factor in the CSF of patients with amyotrophic lateral sclerosis.