Description
Riluzole is a benzothiazole derivative with anti-excitotoxic effects that acts by blocking the presynaptic release of glutamate, indirectly antagonizing glutamate receptors, and inactivating neuronal voltage-gated Na
+ channels (ED
50 = 2.3 μM). Riluzole suppresses glutamate-induced seizures in rats at an ED
50 value of 3.2 mg/kg and displays neuroprotective effects in hypoxic animals at an ED
50 value of 4 mg/kg. Formulations containing riluzole have been explored as therapeutics for slowing disease progression of amyotrophic lateral sclerosis.
Uses
Riluzole is a glutamate release inhibitor. It also induces caspase-dependent apoptosis and suppress cell proliferation in human heptocellular carcinoma. Riluzole is a neuroprotective and a anticancer agent.
Uses
Riluzole is a benzothiazole derivative with anti-excitotoxic effects that acts by blocking the presynaptic release of glutamate, indirectly antagonizing glutamate receptors, and inactivating neuronal voltage-gated Na+ channels (ED50 = 2.3 μM). Riluzole suppresses glutamate-induced seizures in rats at an ED50 value of 3.2 mg/kg and displays neuroprotective effects in hypoxic animals at an ED50 value of 4 mg/kg. Riluzole has been explored as a therapeutic for slowing disease progression of amyotrophic lateral sclerosis.
in vivo
In normal na ve rats, systemic injection of Riluzole hydrochloride (8 mg/kg, i.p.; n=6 rats) decreases the duration of ultrasonic but not audible vocalizations evoked by noxious stimulation of the knee joint compare to vehicle tested in the same rats (P<0.05). Systemic application of Riluzole hydrochloride (8 mg/kg, i.p.; n=19 rats) decreases the vocalizations of arthritic rats compare to predrug and vehicle significantly (P<0.05 to 0.001). Riluzole hydrochloride administered into the CeA significantly decreases the duration of audible and ultrasonic vocalizations evoked by noxious stimulation of the knee compare to predrug values (n=8 rats; P<0.05 to 0.01)[2].
References
[1] B C CHEAH. Riluzole, neuroprotection and amyotrophic lateral sclerosis.[J]. Current medicinal chemistry, 2010, 17 18: 1942-199. DOI:
10.2174/092986710791163939
