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Riluzole is an inhibitor of calcium channels.1 It is selective for the voltage-gated calcium channels Cav2.2 and Cav2.1 over Cav1.2 at 30 µM. Riluzole (10 µM) inhibits increases in intracellular calcium levels induced by NMDA (Item No. 14581), L-glutamic acid (Item No. 30377), or veratridine in primary rat cerebellar granule cells.2 It reduces glutamate, but not aspartate, release from the left caudate nucleus in cats when used at a concentration of 10 µM.3 Riluzole reduces slow wave activity and increases high frequency neuronal activity induced by carotid artery occlusion (CAO) in gerbils in a dose-dependent manner and decreases the CAO-induced infarcted cortex volume in rats when administered at a dose of 8 mg/kg.4 Dietary administration of riluzole (44 mg/kg per day) increases survival time and the total distance ran in an SOD1-G93A transgenic mouse model of amyotrophic lateral sclerosis (ALS).5 Formulations containing riluzole have been used in the treatment of ALS.
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1. Effects of the neuroprotective agent riluzole on the high voltage-
2. Antagonism by riluzole of entry of calcium evoked by NMDA and veratridine in rat cultured granule cells: Evidence for a dual mechanism of action. Br. J. Pharmacol. 113(1), 261-267 (1994).
3. Riluzole inhibits the release of glutamate in the caudate nucleus of the cat in vivo. Neurosci. Lett. 147(2), 209-212 (1992).
4. Neuroprotective actions of riluzole in rodent models of global and focal cerebral ischaemia. Neurosci. Lett. 140(2), 225-230 (1992).
5. Riluzole preserves motor function in a transgenic model of familial amyotrophic lateral sclerosis. Neurology 50(1), 62-66 (1998).