If you can recall a very important correction you once gave me was that protiens don't cross cell membranes. You were so right. In this case the proteases act on the external cell membrane receptor sites (ie. they are extracellular) which then trigger cell death. Thus the effectiveness of AT3.
Right, the caspases that trigger apoptosis are intracellular. The issue might be what extracellular events could trigger cells to activate those caspases and induce apoptosis. If rATIII inhibited the extracellular signalling, then that would reduce apoptosis. This is only pre-clinical data and we need a lot more data to better gauge the prospects. At least GTCB is in the position to provide a lot of rATIII to generate that new data.
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