Apr 30 2014
Anavex Life Sciences Corp. (OTCQB: AVXL), a clinical stage biopharmaceutical company developing novel drug candidates to treat Alzheimer’s, other diseases of the central nervous system (CNS) and various types of cancer, today announced the findings of a research study published in the current issue of peer-reviewed scientific journal Brain. For the first time, scientific data shows that a sigma-1 receptor (S1R) agonist produces functional neurorestoration in animal models of Parkinson’s disease (PD). Anavex is encouraged by the report because its results point to the potential for the Company’s S1R drug candidates ANAVEX 2-73, ANAVEX 3-71 (AF710B) and ANAVEX 1-41 of being disease-modifying treatments for Parkinson’s disease.
“The findings from this new study are very encouraging and may further increase the scope of the therapeutic potential of our sigma-1 receptor agonists, including ANAVEX 2-73, ANAVEX 3-71 and ANAVEX 1-41,” said Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex. “We look forward to exploring preclinical work with our S1R agonist drug candidates in Parkinson’s models.”
Parkinson's disease is a chronic and progressive degenerative disorder of the central nervous system. The motor symptoms of Parkinson's disease, including tremors, slowness of movements, stiffness in the arms, torso and legs, and impaired balance and coordination, result from the death of dopamine-generating nerve cells in the brain. While the majority of existing treatment options focus on symptomatic relief, a disease-modifying drug remains an urgent unmet need in the PD market.
The Brain publication describes how the S1R agonist “PRE-084” produced a dose-dependent behavioral and histological neurorestoration accompanied by an upregulation and activation of cell survival pathways in animal models. A neuroplasticity-boosting action is likely to be the main mechanism through which chronic treatment with PRE-084 alone improved behavior. This study indicates that treatments restoring synaptic connectivity in models of Parkinson’s disease may produce functional recovery independent of an increase in dopamine levels.