2ndst, anything is possible.
As I understand, what the earlier in-vitro test showed was that the circulating Bavi needed enough B2GP1 such that both of the arms would bind to that, at which point they could bind to PS.
When the molar concentration of B2GP1 dorpped lower than about twice that of Bavi, you end up with a bunch of Bavi with only a single B2GP1. And these do not bind.
So back to the trial. It looks very reasonable that at "low" B2PG1 concentrations you see the same effect. The 200 cut would have been something like 10X that of Bavi by my math. BUT one must allow for in-vivo not behaving like test tubes. So I can understand under 200 one might see the "single arm" problem.
But once the B2PG1 is sufficient, the Bavi will be fully bound with B2PG1, so the concentration of Bavi binding would only be dependent on the Bavi itself. And that was not the variable here.
I did consider the possibility that higher levels of B2GP1 were directly competing with the Bavi at the PS sites. If that is what you are suggesting, I agree it would be possible (AFAIK), but looks like a real reach unless we see more information.
As GJH said, this is such an obvious issue you would think they would have had a solid understanding on how B2GP1 effects the PK of Bavi.
Hell, I will accept some mice data if they can shed some light :-)
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