An animal model of experimental autoimmune encephalomyelistis (EAE) designed to replicate multiple sclerosis (MS), was used to study the efficacy of Symadex in both acute and chronic phases of the disease. While treatment with Symadex in this study attenuated acute EAE, it prevented chronic disease.
Importantly, in chronic disease Symadex also demonstrated a statistically significant ability to reverse clinical signs of EAE, including perivascular inflammation, myelitis (inflammation of the spinal cord resulting in a loss of its ability to transmit nerve impulses) and demyelination (the loss of myelin, a protective coating of the nerve fibers, that can lead to impaired bodily functions).
Symadex also increased spinal cord remyelination (the repair of damaged myelin) in the study. In the study, remyelination was determined after four weeks of treatment by a blinded observer who measured the size of all lesions and the amount remyelinated in all sections of the animal. The study also builds on prior data demonstrating Symadex’s novel mechanism of action, which is believed to directly target macrophages and monocytes, key cells responsible for driving the autoimmune response.
Richard Dean, CEO of Xanthus, said: “We remain on track to initiate a human proof-of-concept study in autoimmune disease in 2008 and believe the data on remyelination enhances the partnering opportunities for Symadex.”