>> I had assumed x507 gummed up cross signaling between T-cells by competitive binding. <<
Could well be. But, there are a couple of in vitro studies out there (let me know if you want the abstracts) that suggest otherwise.
I waited for the data on Amevive. Loved the voyage through Biogen Bull that George described, but...... having arrived at our destination, what does it mean for 507?
From the initial description of results by MEDI, one might assume that 507 either works by a different mechanism than Amevive, or that it complements Amevive's mechanism with a second (apoptosis of antigen-activated cells?).
It's a long shot. However, the eventual prize for any MAb that can specifically down-regulate a specific immune response is $5 billion plus. At 10%, the potential BTRN payback is enormous.
So, we can (1) assume that the initial feedback with respect to 507 dosing implies that it won't encounter Amevive's blech re. relative efficacy, or (2) get depressed, throw in the towel, and line up behind anti-CD11a.
Which was are you leaning? Others?? |
