Thanks C.J. There is so much excitement about Bavi's second MOA -- i.e. it's ability to trigger an immune response by covering up PS and thereby promoting chemokines (MIP1a and MIP1b) that facilitate an adaptive immune response to the pathogen -- that it is sometimes easy to forget the original tumor-vessel-destruction science that led to Bavi's development in the first place.
Of course Bavi's second MOA -- i.e. enabling the immune system to recognize and destroy virions and tiny metastatic tumor cells as the foreign pathogens that they are -- is ultimately more important in creating a lasting therapeutic effect.
But if you want to understand why the pending registration trial is likely to generate Overall Tumor Response Rates way above the 6% or maybe 10% remission rate that is needed to get accelerated approval for Bavi in refractory 2nd line NSCLC patients, then it's all about Bavi's first MOA, not its second MOA.
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