Neurological deficits in multiple sclerosis (MS) and in experimental allergic encephalomyelitis (EAE) show demyelination of the nerve fibers, which are responsible for transmission of signals. The myelin appears to be attacked by the cells of the immune system. A viral etiology has been implicated in patients with MS. Oxidized toxins (MN) have been shown over the past 50 years to act as antiviral agents that are capable of inhibiting viral replication, and have shown promise in alleviating symptoms in EAE models of MS. The safety of these compounds has been a factor in their limited use. Development of a modified cobra toxin (MCTX) may prove more beneficial in inhibiting symptoms of EAE. In this study a modified cobra toxin (MCTX) was compared with the older oxidized toxin (MN) in an established EAE animal model. The results show that MCTX is capable of inhibiting the development as well as the relapsing phase of EAE in Lewis rats more efficiently than MN. It is possible that a safe cobra toxin can be developed with therapeutic efficacy for treatment of MS or vaccine development.