RE: R&D spotlight25 Feb 2026 23:02
Episode 14 - 24.02.2026
This is how my transcript reads for the last slide. Adjust speed to 0.75 for clarity then:
16:50 CC: And the tumor can just keep using FAP over and over again. It cleaves and it can cleave again.
So in conclusion (Slide 11), lets pull this all together.
The conclusions from the tumor and plasma PK, very rapid tumor penetration, so the T-max there, we get that early spike in the tumor, the second is we get a much higher, (a log higher!) concentration in the tumor, so you get that initial hit of the drug.
Then finally we have nearly three times higher tumor selectivity of the preCISION delivery versus inHER2.
Then we think that these changes, these PK changes are translating, albeit some of them are subtle, but some subtle differences between the animal models.
So we get anti tumor activity, robust, durable, and reproducible anti tumor activity, even at that really low FAP expression which is what we need to see as we move into the clinic.
And then in terms of FAP overall, one of the nice things about this target FAP is it's stable,
because it's expressed on the fibroblast and not necessarily the tumor cells.
It's really not going away, - so even as we continue to dose our drugs, they're going to get cleaved, even if the tumor dies.
The fibroblast are still going to stick around, so that's the difference in the mechanism of action.
(Ruairidh: 'That's why we are so excited'. - Now look at frame 18:22, and the look on all three faces. CC struggling to remain deadpan.)
We get asked 'well what is the implication of this'.
I think it increases our likelihood of success, - the probability of success of AVA6103, - as it moves into the clinic and gets started in phase one.
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Have we been told all the R&D findings here?
Nope!
However, it's great news for those whose cancer has metastasized.