Dr. Susan Galbraith

So I do think that reflects that, you know, overall,

treating physicians and the patients are learning to manage this side effect over time.

I think it's important just to look at the discontinuation rate on the trials and also the more severe adverse event rates and the rate of fatal events.

We had no fatal events due to adverse events on the tropium breast O2 study.

I think that's important.

Well, we think that the combination of ADCs and immune checkpoint inhibitors is looking very promising in a number of different settings.

We also presented an update on the begonia data set in triple negative breast cancer, which is a combination of our PD-L1 inhibitor, Divalumab, together with Daturae.

in a later line setting with an 80% response rate and really impressive durability and response.

Again, we saw that in both PD-L1 high and low patient populations.

So I think what tropium breast O2 does is it sets the scene for three of the studies that we've got ongoing that are looking at that combination.

The first is the tropium breast O3 study, which is in the post neoadjuvant setting, a bit like the destiny breast O5 setting.

And I think that's going to be an important opportunity because, again, if patients with triple negative breast cancer get metastatic disease, as I've said, their longer term outcomes are much poorer than

for patients with HER2-positive or homo-receptor-positive disease.

So if we can prevent patients getting to that metastatic setting to better treatment in the early stage, I think that will be important.

The second study is the tropion-breast-04, which takes it into the neoadjuvant setting, more analogous to the destiny-breast-11 data that we referred to earlier.

And then we have tropion-breast-05 in the first-line metastatic setting, again, looking at the combination of daturae and divalimab.

So I think with those two studies, we're very much looking forward to the results of those reading out over the next period.

Well, I mean, I think we have to wait and see whether you're getting the effect size that's seen on PFS translate through to similar effect size on OS.

You know, as we said, you know, our strategy has been to take

targets where you can address the same cell, if you like, with two different targets, so like the PD-1 TIGIT or the PD-1 CTLA-4, because we have seen data that suggests that that co-inhibition on the single cells by having it on one bispecific actually makes a biological difference in terms of what you're achieving.