Riluzole is a neuroprotective drug that acts as a sodium channel blocker against the pathological influx of sodium to inhibit abnormal glutamatergic neurotransmission in the central nervous system (CNS). This drug is approved by EMA and FDA, safe and well-tolerated treatment for patients with amyotrophic lateral sclerosis (ALS) [1]. ALS results from the degeneration of upper and lower motor neurons. There is a life expectancy of a patient with ALS that expands two to five years from the time of diagnosis. The time span between the first symptoms and the final diagnosis influences the ALS prognosis. In the early stages, symptoms may go unrecognized and undiagnosed. Riluzole is the only treatment that increases the survival rate of patients with ALS. Research following in vitro models, after excitotoxic action in motor neurons, showed the regression of lesions and the reduction of glutamatergic spontaneous events. [2] Riluzole (C8H5F3N2OS) or 2-amino-6-(trifluoromethoxy) benzothiazole is a durg that falls into the category of benzothiazoles. It has the molecular weight of 234.2g/mol and the melting point of the compound is found to be 119°C. The average absolute oral bioavailibilty of riluzole is 60%, while the drug is approximately 90% absorbed. It will show a linear pharmacokinetics over a dose range of 25-100 mg administered every 12 hours. [3] The chemical structure of riluzole is described in figure 1. TG, DSC and FT-IR studies have been used to highlight the degree of incorporation of the active substance in the membrane and the possible interactions between the drug and the polymer.figureFigure. 1. Chemical structure of riluzole Figure 2. Normalized Heat Flow for membrane and membrane impregnated with rilozole 10 respectivelly 30 mins