Well, it looks like all the very confident longs can't or won't answer. {{Why do you think/believe Bavi is the best and most important immune modulating agent in the world when it has failed time after time in human trials?
PPHM longs keep having their hats on pre-clinical work on cell lines or mouse models. That is a very low bar for any drug to clear. The tumors in mouse models are designed to develop quickly and are more homogeneous than human tumors. In addition, the mice are young and have robust immune systems. The repeated failure of Bavi in multiple human trials means you have to start asking questions like the following on I previously posed.
{{What are the possible negatives aspects of its MOA, especially compared to the strategy of direct modulation of immune cell activity like interfering with the PD-1/PD-L1 receptor/ligand interaction?}}
Bavi has multiple strikes against it in this regard. I believe Bavi has a half-life of about 1 day, which is relatively short. You want your antibody to remain around to mediate its effects, and successful therapeutic antibodies generally have much longer half-lives than one day.
More important/problematic is the target numbers. How many antibody-binding targets are present, and what percentage of the receptors must to be bound by your antibody to elicit the desired response? There are only about 10,000 PD-1 receptors on a T-cell, and so at most that many antibody molecules need to be bound to relieve the PD-L1 inhibition, but the number is likely much smaller.
Bavi targets exposed PS. There are about 1 billion lipid molecules/cell and there are estimates of 3%-10% (30-100 million) of these are PS. How many are exposed on tumor cells? Hard to get a read but Jurkat cells are estimated to have 600,000 PS molecules/cell exposed but this can rise to 25 million/cell. That is a lot of targets for bind to Bavi, and a hell of a lot more than PD-1 receptors on T-cells. You also have to consider that oncology patients tend to be older, and that means lots of cells undergoing apoptosis. Cells undergoing apoptosis expose PS and so act as a sink to draw off the short-lived Bavi antibody molecules. You also have to consider that chemo is going to induce cell death for non-tumor cells, providing another sink for Bavi antibody. Put these together and you might begin to understand why Bavi hasn’t done well in human trials as a single agent or when combined with chemo.
I would rather ask why Dr. Jedd Wolchok at MSK is placing PS Targeting in play with other IO drugs in combo Why would those BP's that back other IO drugs want MSK to combine their IO drugs with PS Targeting ?
I gave a series of reasons to help explain why Bavi keeps failing in human clinical trials. You avoided addressing my points. Instead you repost nebulous explorations which may include Bavi in some small subset as part of a larger approach to examine combinatorial immunomodulation. By PS targeting, I assume you mean tumor cell receptors like Tims, which associate with PS near their cytoplasmic proximal domains. These are far superior targets as they will be much fewer in number.
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