Catalog No.S1614 Synonyms: RP-54274, PK 26124

Riluzole Chemical Structure

Molecular Weight(MW): 234.2

Riluzole is a glutamate release inhibitor with neuroprotective, anticonvulsant, anxiolytic and anesthetic qualities.

Size Price Stock Quantity  
In DMSO USD 130 In stock
USD 97 In stock
USD 970 In stock
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2 Customer Reviews

  • Spatial memory performance. a Latency to find the hidden platform. LPS-infused controls and Aged controls were impaired (*p<0.001) compared to young aCSF-infused rats. The performance of Aged rats improved across days only when treated with Ril (†t=0.035). b Distance. LPS controls swam a greater distance than aCSF controls and Aged controls (*p≤0.036). c Swim Speed. Aged rats swam the most slowly (*p≤0.001). d Thigmotaxis. Aged controls spent the greatest percentage of time within the pool perimeter (*p<0.001).

    J Neuroimmune Pharmacol, 2013, 8(5):1098-105.. Riluzole purchased from Selleck.

    The effect of intrathecal administration of riluzole on changes of tail flick latency in EA-treated rats (Mean ± SD, %, n = 6). EA was given once per day for eight consecutive days. Riluzole or vehicle was given once daily 30 min prior to EA. The significance of differences was calculated by a one-way ANOVA. EA + V: EA plus vehicle; EA + R20: EA plus 20 μg riluzole; EA + R10: EA plus 10 μg riluzole; EA + R5: EA plus 5 μg riluzole; R20, 20 μg riluzole. The values with different letters (a–d) at the same day differ (p < 0.05).

    Int J Mol Sci, 2016, 17(3):357. Riluzole purchased from Selleck.

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Biological Activity

Description Riluzole is a glutamate release inhibitor with neuroprotective, anticonvulsant, anxiolytic and anesthetic qualities.
Sodium channel [1] NMDA receptor [1] Glutamate release [2]
In vitro

Riluzole inhibits the release of glutamic acid from cultured neurons, and from brain slices. 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. Electrophysiologic experiments performed on isolated excitatory amino acid receptors expressed in the Xenopus oocyte have revealed that Riluzole inhibits currents evoked by N-methyl-D-aspartate (NMDA) (IC50 = 18 μM) and kainic acid (IC50 = 167 μM). Riluzole has been shown to stabilize inactivated sodium channels in frog sciatic nerve, in rat cerebellar granule cells, and on recombinant rat sodium channels expressed in Xenopus oocytes (Ki = 0.2 μM). Riluzole also blocks some of the postsynaptic effects of glutamic acid by noncompetitive blockade of NMDA receptors. Tiluzole 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. [1]

In vivo Riluzole can easily cross the blood-brain barrier. Riluzole has neuroprotective, anticonvulsant, and sedative properties in vivo. In a rodent model of transient global cerebral ischemia, a complete suppression of the ischemia-evoked surge in glutamic acid release has been observed by Riluzole treatment (8 mg/kg i.p.). [1]


Solubility (25°C)

In vitro DMSO 46 mg/mL (196.41 mM)
Ethanol 46 mg/mL (196.41 mM)
Water Insoluble

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 234.2


CAS No. 1744-22-5
Storage powder
in solvent
Synonyms RP-54274, PK 26124

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00088699 Recruiting Depression|Mood Disorders|Bipolar Depression|Major Depresssion National Institute of Mental Health (NIMH)|National Institutes of Health Clinical Center (CC) July 26, 2004 Phase 1|Phase 2
NCT03039673 Not yet recruiting Amyotrophic Lateral Sclerosis Centre Hospitalier Universitaire de Nīmes April 2017 Phase 2
NCT02859792 Not yet recruiting Spinal Cord Injury Assistance Publique Hopitaux De Marseille December 2016 Phase 2
NCT02796755 Recruiting Inflammation|Fatigue Emory University April 2016 Phase 4
NCT01910259 Active, not recruiting Secondary Progressive Multiple Sclerosis University College, London|Medical Research Council|National Institute for Health Research, United Kingdom|MS Society|University of Edinburgh|Queen Mary University of London|Keele University|University of Sheffield|University of Leeds|University of Warwick December 2014 Phase 2
NCT02124941 Recruiting Cocaine Dependence Yale University February 2014 Phase 1

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