Replies to post #123217 on Anavex Life Sciences Corp (AVXL)

[F1ash]

I thought WSU already did a pre-clinical trial establishing those things (preservation of oligodendrocytes, etc) for 2-73 and DM? Were they talking (in your post) about the need for future clinical trials to confirm what they found pre-clinically? Or, is it a case that WSU found that 2-73 and DM did impress pre-clinically, they now want to find out what aspect of their MOA's (sigma 1, NMDA, muscarinic) is/are responsible for the positive results?

I believe they did that here:

“ANAVEX2-73 inhibits OL cell death induced by staurosporine (apoptosis), excitotoxicity (glutamate via ionotropic receptors), ROS (induced by H2O2) and a mediator of inflammation (QA) but not nitric oxide or KA. For OPCs, of the toxic agents assessed so far, ANAVEX2-73 also protects from the same agents as found for OL. This pattern of in vitro protection for OL and OPC is the same as we reported for DM (Lisak 2014 et al.), chemically unrelated, but sharing both s-1R agonist and NMDA antagonist functions with ANAVEX 2-73. DM is a non-competitive agonist and ANAVEX2-73 a competitive agonist for s-1R. ANAVEX2-73 is also an agonist for muscarinic receptors and affects Na+ channel site 2. The relative roles of these molecules at s-1 and NMDA receptors and the role of muscarinic receptors and Na+ channel site 2 activity for ANAVEX2-73 in relation to OL and OPC protection is not as yet clear and will require further study. DM, ANAVEX2-73 and future s-1R agonists might have a protective role in treatment of patients with MS. “

Perhaps the next presentation will answer the part I bolded?

http://www.anavex.com/my_uploads/Sigma-1-Receptor-Agonists-Inhibit-Oligodendrocyte-Cytotoxicity.pdf