Morning kpax. Unfortunately that abstract doesn't really address the substance of my quesiton. I'd really like to hear you thoughts about the (potential) conflict I can see emerging in relation to MPL's method of action. ONJCRI recently identified ER stress as central to MPL's anticancer MOA in several cell lines. While they also confirmed MPL's ability to induce autophagy, the drug's induction of ER stress concerns me as numerous studies (I listed some in my previous post) implicate ER stress in ALS/MND onset/progression. As I'm sure you would appreciate, there are many different ways in which ER stress might be induced - so it may or may not be an issue. What I'd really like to hear is, based on your knowledge of cell function and the role of ER stress in neurodegenrative diseases, how do you see this tension resolving? I guess once we have the pharcodynamic results all will become clear!
Cheers
Densy
PAA Price at posting:
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