Great. All right, everyone, thank you for joining us, our fireside chat with Summit Therapeutics. It's a great pleasure to welcome Manmeet Soni, Chief Financial Officer, and Dave Gancarz, Chief Business and Strategy Officer. Before I start, I just want to do a quick, let's just check, for anybody who, you know, who wants to ask a question here, please feel free to scan the QR code and we can ask a question on your phone and then it will transfer over to my iPad here and then I'll ask a question. Feel free to ask away any questions that you might have. All right, with that out of the way, Manmeet, Dave. Really, really a pleasure to have you. Welcome to the UBS Healthy Conference. Thank you. Appreciate you having us. Great. Thanks, David. Thanks for having us. Excellent. Maybe just to start from a high-level perspective, you know, of course, Summit is a very topical name. Everybody cares about now. Could you just provide a kind of high-level overview of Summit, you know, your lead molecule, ivonesimab, and the overall strategy for the company? Yeah. You ready? Yeah. Sure. Yeah. Thank you for the question. I think overall, our lead molecule is ivonesimab. It is a PD-1/ VEGF bispecific antibody. This is our lead and primary focus of Summit Therapeutics. From a background perspective, Bob Duggan and Maky Zanganeh are our Co-Chief Executive Officers, as well as the rest of our management team. Manmeet and I are here, Fong Clow and Urte Gayko. When we look at the opportunity of what Summit is looking to do, it is focused primarily on bringing the mechanism of a PD-1, the mechanism of a anti-VEGF together into a single molecule, and creating a novel mechanism through which. We target both PD-1 and VEGF, but the molecule itself was specifically engineered to really exceed what both, both previously established targets do into a new mechanism that's primarily driven by a couple of factors. One, ivonesimab, being a tetravalent bispecific antibody, has a shorter half-life. What that does is really emphasize the safety of the compound. When we look at some historical considerations for anti-VEGF therapy that have had higher risks of bleeding, proteinuria, and hypertension, that have ultimately been results of accumulating toxicity that maybe have reduced some of the opportunities for overall survival, ivonesimab was designed to, with a shorter half-life, reduce that risk. Finally, cooperative binding is a key component of this. In the presence of VEGF ligands, the affinity or the binding of ivonesimab to PD-1 is about tenfold stronger than, in and of itself, you know, a traditional PD-1, if you will, without the presence of a VEGF and the VEGF binding. What that allows for is really the hypothesis being that that is most effective in the tumor microenvironment where both PD-1 and VEGF exist. That really attracts the molecule to be on target at the tumor to help ultimately slow disease and, and ultimately kill the tumor cells. You know, the ultimate goal being to increase survival for patients. If we move earlier and outside the metastatic phase, increased cure rates would be the intent. Got it. And that's really helpful here. Great. We can move on to some of the key trials. You know, you do have multiple trials including HARMONi, HARMONi-6, you know, HARMONi-2, and others, right? Let me start maybe talking about the HARMONi-I, and then the most recent update from SITSI, which is a HARMONi- A trial where you guys provided some updated data in overall survival that showed a hazard ratio of 0.74, which is, you know, statistically it's like 0.019, right? This helps us contextualize that data here. You know, Dave, what does it mean for you? And also at the same time, how do you think this data kind of translates into HARMONi- I, which was recently presented at WCLC? Yeah. There are four phase threes that have read out with respect to ivonesimab. The first trial, in all four of those, were positive readouts. Four phase threes that have read out, four positive phase threes. When we look at the opportunity in HARMONi- A, that was the first trial that was initiated from a phase three perspective, right? That ultimately, on Friday, as you mentioned, resulted in a statistically significant OS benefit. Contextualizing that, if we think about, and this was part of what we spoke about at the beginning, what was HARMONi, what was ivonesimab designed to do? It was really to increase, you know, the potential of duration and quality of life of patients. In doing so, the half-life of ivonesimab is intended to make a more safe molecule as opposed to the individual compounds. What we hear historically, the notion is that if you anti-VEGF, when you accumulate duration of therapy, you ultimately accumulate toxicity and that prevents survival. This really was intended, this showed that that's not the case for ivonesimab. This was the first phase three study. It was a statistically significant OS benefit now. This is a place where PD-1s have failed historically. PD-1 plus VEGF has not shown an overall survival benefit. This really puts to rest the notion that a PD-1/VEGF bispecific will not show an overall survival benefit. Full stop. In addition, you asked about the translation to HARMONi, the global study. What we saw there as well was, the data that we presented at the World Conference on Lung Cancer, World Lung, in September, we showed a longer-term follow-up of overall survival as well for the global patient population, right? HARMONi- A specific to China, HARMONi global population. That had a nominal p-value of 0.03, which would have been below the statistical cutoff for survival in that study. What we show is that the mechanism is very much bringing, you know, an additional enhanced benefit to those patients. We think the benefit-risk profile, you know, is reflected in both of these studies now. It also shows the consistency of the data. When we overlay the curves from HARMONi- A and HARMONi, extraordinarily consistent in terms of the overlap. We showed at World Lung as well the consistency of those curves, from a PFS perspective as well when we added in additional patients from the West. Yeah. I think in total, I think that kind of covers the translatability and the opportunity. Yeah. If you go back, like 18 months, two years, there were a lot of open questions, right, which all investors had. And all of them have been mostly answered, right? The first one was, guys, can Chinese data, you know, replicate into Western? We have shown that, right, through HARMONi, right? Will PFS translate into OS? We have shown that also, right? And will OS be consistent, right? Like, on maturity, will OS not deteriorate? We have shown that through HARMONi- A, right, which it used to be 0.80 and after, for the follow-up, it's now 0.74. All those questions which were there have been answered, right? Western versus Eastern, PFS to OS, and OS to further mature OS. Yeah. Now, do you attribute that, you know, the difference in terms of OS, you know, where we saw a benefit and statistically significant, you know, OS in the HARMONi- A trial, whereas, you know, the HARMONi- I trial, although it, you know, the nominal p-value is less than 0.05, you know, the first analysis that you, the primary analysis was not, right? Do you attribute this to the statistical plan, the powering, or how, how do we think about this? Timing of enrollment, right? The Western patient data was not matured enough. Once we did the mature data for Western, it was significant. It cannot be called fat significant because now we have used alpha and done that. It is a statistical issue. The drug is working as it was engineered, right, as we were saying. The drug demonstrated, but you will have to wait for the appropriate follow-up of the patients, right? You cannot have eight, nine months mature data to show OS benefit. Once we reach 13,14 months of follow-up, it converted into, you know, showing a significance. I think there was an understatement on the expectations when we started this trial in terms of what it takes to bring a trial directly into phase three in the U.S. and Europe where it had not been previously exposed. If you think about the factors here, right, we had a, obviously, we did the deal in end of 2022, beginning of 2023, and had a lot of confidence in the opportunity. That is why we started immediately. For physicians, this, they had not been previously, you know, working with the drug. This was, you know, we are effectively asking trust the data that we had been, generated. Now, today, over 40,000 patients have been administered ivonesimab, either 3,000 or so in a clinical trial setting. When you include those in the commercial setting in China, over 40,000. At the time, you know, we had several hundred patients, but all from China. We were asking physicians to trust the data from China. There were, as we talked about, concerns with respect to VEGF tolerability. Is this something that leads to bleeding risk? Are there additional risks for patients? We were able to, you know, demonstrate through putting a few analyses together and then ultimately, you know, further data readouts that the risk was much lower. When you look at the specific factors for EGFR-mutated lung cancer, brain metastasis is a common location of metastasis. TKI is effective in slowing down progression of brain mets. We did not have data that had been published at that time with respect to control of brain mets. We've now, you see the published curves, PFS and OS with those patients with brain metastases entering the trial. You know, we see that that has been something that, you know, ivonesimab has shown an improved hazard ratio for those patients with, you know, existing baseline brain metastases. Finally, we're still working through, you know, a lot of sites. We're still working through some of the ramifications of COVID in early 2023 in terms of fully gearing up their staff back and whatnot. That led to, as Manmeet talked about, that four-month delay or so. When we did that ad hoc analysis at World Lung, that four months later on follow-up, you saw the p-value that was attributed to that study, the nominal p-value. I think another thing to add, might be in different words, is when you generally are doing a phase three, you had some experience in the United States, right? Because we had got this drug from China, there was zero experience, right, with that drug. We had to open up the sites. The company was just starting up, right, to open up the sites, get the operational delays in getting the CTAs up and sites up. It takes time, right? That was the few months delay, right? Now it's like now we have announced that we are enrolling so fast on squamous and even non-squamous on HARMONi-3. Right. Yeah. It's different now after 18 months, two years, you know? Right. It's ironic when you look back, I think. People talk a lot about the PD-1/VEGF class. We talk about the other big pharma who were very interested. Only a short period of time ago, all of that was a bit different in terms of the climate, the experience, and the perceived opportunity at the time. Got it. Yeah. And that's really helpful. Then, regarding the HARMONi- I BLA submission, which I think caught many investors by surprise here, you're saying that you're actually planning to submit in 4Q. I was curious around the decision to do that. Have you met with the FDA? Have you got buy-in from them regarding the submission? You know, how confident are you that overall package at the FDA will lead to an approval? Yeah. We have a ton of respect for the agency. We've announced or started four phase three clinical trials. That obviously comes with a lot of meetings with the agency across a bunch of divisions as well. What we don't do is get into meeting-by-meeting discussions in terms of what we have. What we made the conclusion on was really the benefit-risk profile that we saw with ivonesimab considering what's the historical precedent, what's been approved historically. There are no regimens with statistically significant OS benefit that have been approved in the U.S. in this setting. You know, we look at the tolerability of ivonesimab plus chemo in this setting, and we see a very manageable safety profile. That risk-benefit profile, you know, in consultation with many folks, in many different areas, physicians, and so on and so forth, this became the path forward that we wanted to take. Got it. And for the BLA submission, do you expect the FDA to have a later data cut of the OS for the submission? Similar, similar to what I said. I think we don't, we're not gonna presuppose what the agency will do. We, we ultimately, we have an extreme amount of respect for the agency as well as the process to go through that, you know, whether it's the pre-BLA, the BLA process, and whatnot. We'll have multiple engagements throughout, but we're not gonna give kind of step-by-step through that. We'll certainly work with the agency. To answer your question in different words, right, if they will ask, right, yes, we will. Mm-hmm. Do another cut and provide them, right? We generally have to do that and follow their advice and their questions. Yeah. That's fair. Great. Let's switch gears and talk about HARMONi-6 data here. HARMONi-6 is the China trial for ivonesimab plus chemo versus atezolizumab plus chemo in frontline non-squamous non-small cell lung cancer. Squamous. I'm sorry. Yes. Squamous. Yeah, my apologies. Squamous non-small cell lung cancer. It just helps to understand, you know, contextualize the meaningful efficacy there, and, you know, what does it mean for, you know, for, let's say, reachability to, you know, the global HARMONi-3 trial there? Yeah. I think you know that, right? Atezoli, right, is pretty comparable to Pembro, right? It's in China. And that trial, like, if you're comparing with PD-1, you know, showing a 0.60 hazard ratio, 40% improvement in PFS is huge. That gives us confidence, and readout on a HARMONi-3, which we said, right, we will be completing enrollment for that in the first half of 2026, that, it's, it's looking pretty, you know, stronger in our view. I think the other, so continuing on, on that thought, right, I think we saw HARMONi- A reads out, and it's against placebo, and albeit in an indication that PD-1s had been ineffective. It was, okay, you need to go against PD-1. Then HARMONi-2 reads out, and PD-1, versus Ivo head-to-head, and that being Pembrolizumab beat it head-to-head. When you add chemo, that rising tides raise all ships. That'll dilute the effect. Decisive, you know, statistically significant, clinically meaningful PFS benefit over PD-1 plus chemo. Frontline now, this is the frontline undisputed standard of care in terms of both squamous and non-squamous patients, right? Mm-hmm. Squamous, you know, this is very much comparable in terms of the results of Pembro, Tezli, so on and so forth, Simiplamab. They've all shown reasonably consistent results here in terms of the PD-1 category. Now you take that the next step with respect to the safety profile, right? Anti-VEGF, again, accumulating toxicities, and in particular in squamous patients where it's effectively contraindicated because of the, you know, very high risk of hemorrhagic events, grade three to five, bleeding risk, so on and so forth. We not only show a victory in terms of the trial from an efficacy perspective, but also the safety was incredibly important here. This is a randomized phase three study against PD-1 plus chemo in squamous lung cancer patients. These are patients who are not necessarily highly pre-selected either in terms of risk criteria, so central lesions, cavitated lesions, surrounding major blood vessels, right? This is not a cherry-picked profile as well. What we saw was a very manageable safety profile. Oftentimes between the two, Ivo plus chemo or Tezli plus chemo, it was difficult to tell which was which. That is also extraordinarily reassuring in terms of, you know, going back a couple of years and people saying, "Hey, VEGF, there's a risk. How do we mitigate some of those safety risks?" This is a great example of the tolerability and the manageability of Ivo. How should we think about the PFS benefit will translate to OS benefit there going forward? You know, Dave, you mentioned about this, you know, the short half-life, you know, where we play improved tolerability there. Do you just help us understand? And then, you know, the other flip side of the argument is, you know, there might not be contribution to PD-1 arm. I'm just curious in terms of your thoughts around the, you know, PFS to OS translation ultimately. Yeah. I think the HARMONi- A study for one, showed directly that a PFS benefit leads to an overall statistically significant overall survival benefit. I think now that argument becomes a little bit tougher with a SATSIG OS benefit. I think the other piece becomes what's the rationale why it won't, right? 'Cause I, in some ways, I almost wanna turn that question around. We say, "Hey, why, why do we think it will?" If we look at what are the concerns? Again, VEGF toxicity accumulates, you know, shorter duration of treatment. Ultimately, those toxicities can lead to earlier deaths. We didn't see either of those. We saw a duration of response that was longer. We saw a higher overall response, and we saw an increased PFS benefit. We also saw an increase in a PFS curve that continued to separate further, right? I hope everyone's okay. With that, you ultimately, you know, you see the first trial run lead to a statistically significant benefit. We talked about HARMONi, the global study, and with the pre, you know, what we had believed would be the follow-up time for when that analysis would take place, nominal p-value under the threshold. We're seeing HARMONi-2 at an early ad hoc data cut that was requested from the Chinese health authorities already showing an OS hazard ratio under 0.8, a generally accepted clinically meaningful threshold. We are seeing very positive, albeit early results in terms of the HARMONi-6 study without the toxicity and with a growing benefit across all of the major early endpoints here, if you will. It becomes in some ways difficult to believe that that is not something that translates into OS instead of the other way around in terms of why not. Got it. In terms of the other debate, which is that, you know, thinking about the China to global trial translation, there's a lot of skepticism around, you know, how likely will a China trial, you know, translate in terms of global trials? I'm curious in your thoughts around, you know, any kind of updated data or anything you've seen so far that would give you some confidence around the translation from China trial to global trials. How many was that, right? How many was, you know, from HARMONi- A to HARMONi? I didn't replicate it. If you see in North America, the OS was exactly similar, right? PFS was exactly similar, right? If you look at those graphs, right, they're totally so much overlapping over there to translate. You have to wait for the next one. HARMONi-3 will read out next year to do that, right? Yeah. In addition to what Manmeet said, if you look at median overall survival, 17 months versus 14 months in the West, 16.8 months versus 14 months in the East, right? I mean, effectively the incredibly consistent. Mm-hmm. Median overall survival. You look at, so let's, let's look at, for example, on this one. At the same follow-up time, right? In HARMONi- A at ASCO 2024, at about 50% data maturity, 52% of events that took place, hazard ratio 0.80. That included those who didn't receive a third-gen TKI. We've seen about a 0.02 difference when you exclude those patients, right? If you pull those patients out of HARMONi- A, it's about a 0.82 at that point in time. Pretty much exact same follow-up in the long-term Western follow-up that we presented at World Lung, 0.84. You're talking 0.82, 0.84 at that same about 50% of events time period. Incredibly consistent. The PFS curves as Manmeet talked about, as soon as you add in, you know, more longer-term follow-up on those Western patients, the curve doesn't move. Same with OS. You can overlay the HARMONi and the HARMONi- A curves. If there were a difference in terms of the way patients reacted, you would see fundamentally different shapes. 38% of patients from the HARMONi trial are from the West. 38% of patients acting differently will absolutely change the curve. Got it. Okay. Great. In terms of the next steps for HARMONi-6, could you maybe just share some of the thoughts around, you know, when should we next, you know, expect next data out of OS data or PFS data? Yeah. I think importantly that trial is sponsored by and conducted by Akeso. So that is, you know, mainly for them. I think the, you know, there's been some, the publication in terms of the Lancet had a little bit more, indication with respect to statistics. So that looks like something, you know, that comes at some point next year. But that's really for, for the for the team at Akeso to give specifics in terms of that guidance. Okay. Great. Moving on to your global trial HARMONi-3, you recently amended the protocol to increase sample size for both the squamous and non-squamous non-small cell lung cancer, where each cohort now is powered separately. Could you provide some clarity in terms of what you saw in terms of enrollment rate, physician feedback, and any other clinical data that made you decide to amend the protocol there? Enrollment has been going pretty, you know, fast. That's why we guided, in October only that we will be able to finish squamous enrollment, by, you know, first half of 2026. And non-squamous, you know, which is now 1,000 patients, it's double the size, right? Because squamous patients is 1/3 of the front line and non-squamous is 2/3 of the population. so that's why they are powered separately to see that 600 versus 1,000 patients. But non-squamous is also we started only this year, and we are saying we'll be finishing the enrollment right, in second half of 2026. Enrollment is going pretty fast. That gives us the confidence. That's why the readout for squamous could happen in second half of 2026, for squamous, and non-squamous readout would be in early 2027. Any kind of physician feedback you've been hearing so far on the enrollment, on the receptiveness, receptivity of IV? Yeah. We We had a lot of calls with all our, you know, sites. We have now so many sites up and activated, all positive feedback. They were all, you know, surprised with the outcome of the data and the, you know, ivonesimab have always right work. So we are not seeing anything, all positive feedback from physicians. Their enrollment is going pretty fast. I think. No, I think the only thing I would add to that is agree with everything Manmeet said. I would also add it decreases regulatory risk here. So it increases the probability of regulatory success here. Oh, by splitting it out, right? By splitting out the two into individual cohorts, right? You never want one to look a little bit better than the other. Then you ask the question, did one drag the other one across the line? We started squamous a little bit earlier. I think part of this becomes let's have clean ITTs for squamous and non-squamous, power them both individually. That way, you know, when we look at the analyses, they are, you know, very clean. You can look at the, you know, we've had a lot of topics of conversation, you know, in terms of, in this, this being more a more general comment, but the FDA really wanting to make sure that U.S. patients reflect the overall global patients' results that we see in the trial. We've seen that across a couple of AdCom meetings or ODACs that the FDA's held in the past year. This splits out the populations between the squamous and the non-squamous. That'll make everything a bit cleaner in terms of review and not have any, you know, implied questions that can come. These are very important settings for ivonesimab and for Summit as a whole. This becomes important to be as clean as possible here. Just to clarify, by separating them out, you're actually able to de-risk the regulatory side of things, right? You're able to separately submit the BLA submission with respect, right, of other success of the other trial. That's exactly right. Think of it as two clinical trials within one protocol, if you will. It accelerates the opportunity for squamous to come faster, almost a year faster, because otherwise you have to wait till the end of 2027 if you do combined analysis. Mm-hmm. Anything to share on the powering assumptions for the trials there? I don't think so we have discussed any powering assumption. Other than to say that they're both squamous and non-squamous are adequately powered for both PFS and OS primary endpoints. Yeah. It's interesting. And then you also mentioned that you're able to get PFS data, you know, for squamous, and at the same time you're able to get interim look of the OS. So could you help us understand what's next steps from here? Are you able to file for approval after, you know, if you're able to show, you know, data in second half 2026, you're able to approve, or are you able to submit data right away, submit it for approval right away? Assuming positive data, right? That would be the intent to submit it for the BLA. Yeah. It's It's a total package, you know, question that exactly as Manmeet said, it's we have to review the data. And if that data supports, then that would be the decision to make at that time. Our confidence increased, right, because of the HARMONi-6, right? HARMONi-6 squamous. Yeah. PD-1 plus chemo, right? That told, tells you that, guys, the drug is working in squamous patients and our mechanism of action, which was engineered, right, for that half-life and the cooperative binding. It's working exactly how it was planned and engineered. Got it. Great. Then, moving to HARMONi-2, the China trial, for ivonesimab monotherapy versus pembro. You know, we've seen the PFS data. We also saw the interim OS, you know, 39% maturity. Anything you can guide on in terms of when should we be expecting the OS data, you know, for the final analysis? Again, that's an Akeso sponsored study. At that point, I'll let the team at Akeso provide any updates with respect to that guidance. Obviously, it was really an administrative ad hoc look at that OS look when the CDE was looking to approve and the NMPA ultimately approved that indication. I'll leave it for the team at Akeso in terms of updated guidance there. Great. Okay. And then, you know, you moved recently into a CRC, which, you know, it's great to see that. And indication expansion. You know, maybe you can just tell us a little more about the clinical trial design and powering assumptions and potential timeline for enrollment and readout. We're just getting ready to start at this point. I appreciate the readout and the next steps question there. Look, we're very excited. I think we gave a little bit of detail in our press release and 10Q, but currently, you know, structured at 600 patients with a PFS primary endpoint. I think the place where I would focus that really though is if you take a step back, right? Because I think I'm anticipating your question, but it's, you know, with this, how do you think about where this goes? Now you're going beyond lung cancer, right? If I step back a little bit, this becomes, and just look at ivonesimab, right? There's 14 phase three clinical trials right now, four being conducted globally now, including the CRC, and then 10 being conducted by our partners at Akeso in China. Four of them have read out. Four of them are positive studies. Great backbone. What that 10 implies is really that there's multiple additional places we can go. CRC is one of the places where Akeso is also running a phase three study. You get into head and neck, you get into pancreatic cancer, you get into triple negative breast cancer, additional spaces within lung cancer, biliary tract cancer, so on and so forth. There is a multitude of different places where this drug can go. Another piece that might have been slightly overlooked with respect to HARMONi-6 is the consistency by which ivonesimab performed in that trial compared to the phase two trial. That AK112201 study, 11.1 months of median PFS, 11.1 months of median PFS in the phase three study. You typically have that drop off from phase two to phase three and whatnot. That is not something that I expect will happen every single time by any stretch. When I mentioned at the beginning, 3,000 patients have been administered ivonesimab in a clinical trial setting. Obviously, a lot of that data has not yet been published. What it shows us is the consistency of the impact of ivonesimab, the different settings in which ivonesimab can be impactful, in all of the places that ivonesimab has the opportunity to go, in addition to where even those 14 phase three clinical trials start. We have an opportunity, and we mentioned this during the earnings call. We have the opportunity to expand into a multitude of places, and we plan to do so in the shorter term as well here. This is, we're not done with CRC, and then we're going to take a break. We're going to prepare to continue to expand that plan because this is what the drug deserves. Yeah. I mean, speaking of which, I know we have three minutes left, but I do want to ask some questions around the competitive landscape, you know, as you can imagine. Sure. As the competitive landscape is picking up, you know, it's getting really fierce with, you know, Pfizer jumping on, and BioNTech also has a competitive, you know, PD-1 and VEGF program as well. They're all going after different indications right now. They're potentially, you know, adding different combination strategies with, you know, ADCs and others. Curious your thoughts around, you know, how are you, you know, how are you viewing the competitive landscape and how are you staying ahead of the curve in terms of, you know, developing ivonesimab? Yeah. It's a great question. I think we need to continue to expand the places that we look. That's what I was just speaking to in terms of all of the trials that are being run in lung cancer, the opportunity to go into colorectal cancer, and now expanding, you know, continuing further within the solid tumor space. In addition, combinations are and will continue to be important with respect to treating solid tumors. I think we have a competitive advantage in the sense of, and we're evidencing this with our collaboration with RevMed. We're taking ivonesimab and combining it with multiple RAS inhibitors from RevMed. Those patients will begin to receive that combination in early 2026, right? That's not the only time we'll do that. I think we've been very clear. We'll continue to expand the number of clinical trial collaborations that we have by following the data. There's no chemotherapy backbone that's the standard of care across all solid tumors. We don't believe that there'll be a single ADC platform with a single payload that'll be the standard of care across solid tumors. We've seen many places where, you know, platform A has worked in one type of tumor, but not necessarily another. Then platform B has worked there, but not in the third place, right? Solid tumors biologically are very different. I appreciate that we put solid tumors around all of them, but they're biologically extraordinarily difficult. We see PD-1 work in some and not all, right? What we can do is really follow the data and continue to expand the number of different novel, novel combinations that we do with ivonesimab. That positions us extraordinarily favorably in terms of where we can go quickest without being encumbered by our own pipeline, if you will, in terms of looking to find synergies within our own portfolio. Obviously, there are, you know, there are other companies who see where the puck is going. We see this now readout with HARMONi-6 that gives a lot of confidence in terms of HARMONi-3. As we look at non-small cell lung cancer going forward, could ivonesimab be part of that, you know, standard of care backbone? Now other companies are, you know, can reach out and say, "Hey, as we're looking to get into that space as well, this might make sense for, for combinations. Got it. Great. You know that, right? Checkpoint inhibitor market is expected by 2030 to be over $90 billion, right? There will be competition, and you should expect that. You know, lung cancer is there, right? Non-small cell lung cancer, colorectal, they are big markets, right, to play. Mm-hmm. We think we are not saying we are taking the 100% market share also, right? It is good to have competition, and it is good for patients, right? Absolutely. That's, yeah. Great. All right. Great. One last question. Just over the next 12, 18 months, what should be, what are some catalysts we should watch for? HARMONi- 3 is a big one, right? Right. Squamous will, you know, you'll get the readout, right? The first global trial, which people have been waiting. Again, all the questions which we have answered in HARMONi will be again answered through HARMONi-3, right? BLA filing, right, for EGFR. Those all will come in 12 months. In 18 months, you get HARMONi-3 non-squamous. Further updates on colorectal and few expansion opportunities in the pipeline. We're not stopping anytime soon. Yes. That's great. Catalyst after catalyst, right? Yeah. Don't stop. Just keep going. We have to. We love it. We have an obligation. We have taken responsibility to bring this medicine to patients who are in need. Excellent. Okay. Yeah. Great. I think with that, we can wrap it up here. Manmeet, Dave, thank you for joining us here. Thank you for having us. Thank you for having us. Appreciate it. Thank you.