Etzer Darout: Great. Thanks for taking the question. So thank you for laying out sort of the IND plans for Exelixis. But just wondered if you could comment at all on sort of the phase one assets that you have in development and maybe for 2024 where we could see potential proof-of-concept in the clinic with assets like CBX-12, the ADU-1805 compound and some of the other assets that you have in phase one early clinical trial, I guess, is sort of where we could see potential proof-of- concept there. Thank you.
Amy Peterson: Hi, Etzer. Thanks, it’s Amy. I’ll take that. So we do have some other assets that are partners that are in phase one and we are actively always looking at the data and we’ll make database decisions on how those progress and move forward. But those are good partnerships with our XBOO2 that is advancing into its expansion cohorts. I would say we’re in the process of understanding really proof of developability and the way I differentiate proof-of-concept from proof of developability is proof-of-concept, you have a couple of responses and it’s interesting or you hit a PARP dynamic marker. It looks like the drug is doing something to the tissue in the human, but you don’t yet know how to move that into a pivotal study.
These expansion cohorts for XBOO2 will actually, are designed to actually inform us if we see a certain amount of activity, how would we move into pivotal studies? And so those expansion cohorts are enrolling when they mature and when we have that data is just dependent on how long it takes for the responses and the durability of the responses. So we could have some things in 2024. And then for XL, the USP1 inhibitor, right? That’s just getting started. And as we transfer that in and we go through dose escalation, I think we’ll have a better understanding of what we need to see in terms of proof of developability there. I think we already have a good head start understanding the patient population that is most likely to respond to this sort of an agent and harnessing that knowledge in terms of our eligibility criteria will help us understand how we might quickly move into full development with that asset.
And I think I’ll stop there.
Operator: Our next question comes from the line of Chris Shibutani from Goldman Sachs.
Unidentified Analyst : Hi, this is Steven on for Chris. Thank you for taking our questions. Two from us. On the CABINET, the data that was presented at ESMO showed quite a clear PFAS benefit, though the OS curves didn’t separate as much. So I guess in that light, how confident are you that regulators will view that data package as an approval data set? And then on XL309 recently and licensed, can you speak to what gives you confidence that that could be a best-in-class asset among competitive USP1 inhibitors? Thank you.
Mike Morrissey: Okay, good. So Amy, why don’t you take the CABINET question and then Dana can speak to 309.?
Amy Peterson: Yes, thanks for the question, Steven. It’s an important question to bring up because the way the study was designed is that crossover was allowed. And the study wasn’t blinded early due to the significant benefits and progression free survival that was observed and all patients at that point in time were crossed over. So there’s not really an expectation for survival for us to observe survival. Whether or not that passes the test of the agency is a discussion we’ll have. We’re pretty optimistic given that this is such a rare disease and a high unmet need in late lines of setting where patients really have nothing else available to them. So we’re optimistic. But again, we have yet to have that initial discussion.
Mike Morrissey: Great. Dana, 309.
Dana Aftab: Yes, thanks for the questions, Steven. Regarding 309. So even though that’s an in license compound, we actually did quite a bit of experimental work ourselves in our own labs with that molecule. We have quite a data set that supports our statement that we believe it to be best-in-class. And so similar to what I just said about XL495, we’re planning to give a lot more detail at R&D Day, so just say stay tuned for the update there. We’ll see a lot more. You’ll get a lot more information on the module
Operator: Our next question comes from the line of Joe Catanzaro from Piper Sandler.
Joe Catanzaro: Hi, everybody. Thanks for taking my question. Maybe just a quick one from me. So Amy, I know you have some ADC experience and some prior roles. So just wondering how you think about the next gen Tope 1 tissue factor ADC that you guys have in the pipeline relative to XBO2 and maybe more generally how you think about [inaudible] and tubulin-based payloads versus topoisomerase-based payloads and maybe how you develop these two programs sequentially. Thanks.
Amy Peterson: Hi, Joe. Thanks very much for the question. Thanks for the welcome. Yes, I definitely have some experience in ADC. So with regard to the Typo-1 payload, I think it’s actually an opportunity to take a molecule which, into tumors that both express tissue factor and are sensitive to topoisomerase inhibition. So not all tumors that express tissue factor are sensitive to anti tubulants like or statin. So adding a different payload actually allows us to potentially cast a wider net with regard to some of the tumors that we might pursue. And of course, would offer a differentiated toxicity profile. When it comes to the or statin versus MMAs, there are certain toxicities that are similar. For example, [inaudible], but there are other toxicities that aren’t as similar between our payload and what you might expect from TIPDEC.
So neuropathy and bleeding are not something that we would expect to see with ours. So the payload is different for our XBO02 than what is with TIPDEC. We’re already starting to have a differentiated toxicity profile. We’re excited about the data that TIPDEC has shown, and that offers us an opportunity to think about how we might bring XBO02 forward into that space leveraging our differentiated toxicity profile. So I hope that answered your question.
Operator: Our next question comes from the line of Stephen Willey from Stifel.
Stephen Willey: Yes, good afternoon. Thanks for taking my questions and just a couple of quick clinical ones for me. So on STELLAR-305, I’m just kind of curious. I know Merck announced the LEAP-10 trial didn’t hit its end point I guess a couple of months ago and just curious how you think about Zanza differentiation relative to [inaudible] within the setting of head and neck. And then maybe just a quick follow-up to Joe’s question. I know for JEWEL-101 you’re not looking at cervical as part of any of the combination expansion cohorts. And I guess just kind of given some of the concern around combining Tivdak with BEV and the overlapping bleeding risk, just kind of curious why that’s not on your radar screen right now. Thanks.
