A comparison of riluzole and edaravone for the treatment of amyotrophic lateral sclerosis

The exact mechanism for the pathogenesis of amyotrophic lateral sclerosis (ALS) is not known. However, a number of causes have been suggested in contributing to the pathology of ALS, including oxidative stress, excitotoxicity, mitochondrial dysfunction, aberrant protein accumulation, imbalance in calcium homeostasis, and inflammatory responses. ALS is either sporadic or familial. A number of mutations in genes have been associated with the familial form: superoxide dismutase 1 (SOD1), transactive response DNA-binding protein (TARDBP), chromosome 9 open reading frame 72 (C9ORF72), and fused in sarcoma/translated in liposarcoma (FUS/TLS). In the United States, the two Food and Drug Administration (FDA)-approved drugs for the treatment of ALS are riluzole and edaravone. Riluzole participates in glutamatergic transmission and has been previously shown to decrease excitotoxicity. Edaravone is a radical scavenger that decreases the generation of reactive oxygen species (ROS). In this thesis, clinical trials and scientific studies involving riluzole and edaravone were analyzed to compare the efficacy of these two drugs. In clinical trials, riluzole appears to prolong life in the early stages of ALS, whereas edaravone appears to only slow symptom progression. Making a decision between these two medications involves considering how each one exerts its effects as well as the efficacy of each one in clinical trials