Good morning, everyone. I'm Tara Bancroft, one of the senior biotech analysts here at TD Cowen, and I thank you very much for joining us at TD Cowen's 45th Annual Healthcare Conference. So, for our first corporate session today, we have a fireside chat with Merus. And from Merus, we have Bill Lundberg, the CEO, joining us. So, Bill, thank you very much for being here with us. And before we get started, I just want to say to the audience, if you have a question, just raise your hand, holler out, and we'll make sure you get heard. And I'll repeat the question before Bill answers. So, Bill, I guess you could start with maybe a general overview, any updates that you want to get us level set on before we get started on Q&A. Yeah, thank you. Can you all hear me? If you can't hear me, raise your hand. The first thing I want to start with is simply to thank Cowen for the relationship we've had over the years and continued support you and your whole team provide to us. It's really great. Really appreciate the support. Also want to just caution that I may be making forward-looking statements, and I'd refer you to our disclaimer slide in our corporate presentation, which has the appropriate disclaimers and details that are relevant for this conversation today, too. Okay, so this is a really exciting time at Merus. We're an oncology-focused company with multiple clinical stage assets in oncology of our own and a number of them with our partners and licensees as well. We've been innovators in the field of multispecific antibodies for more than a decade. There are many, many different kinds of multispecific antibody platforms, but we have a particularly unique approach to making medicines. And that is that we try to make them following the tried-and-true approaches of monoclonal antibodies. The reason that's important is because we know how to make really good, commercially successful medicines out of monoclonal antibodies. And we generally think that the more new stuff we take on represents additional innovation that we might have to make, which also represents risk. And we like to systematically identify, evaluate, mitigate, and discharge risk in all of our approaches, whether it's how we think about targets or development of new molecules. And so, as such, our specific flavor of making bispecifics allows us to make a bispecific antibody as a fully human IgG1 antibody coming out of a single cell, so monoclonal. With that, we can do all of the tools and tricks and approaches that monoclonal antibody discovery and development can do. We can do true high-throughput screens to let the biology select what's the best thing that we want to study or what's the best bispecific antibody given a particular target or target pairs. We can do all of the Fc domain engineering, so enhanced ADCC or stealth silencing for T- cell engagers. We can use standard, well-established process development and global commercial manufacturing capability to make our molecule. While leveraging all of this monoclonal antibody approach is a really cool way to make medicines, and we think that it doesn't necessarily guarantee success in the clinic, but we think it improves the chances. Now, when you look across our pipeline and portfolio, for a small company, our pipeline has been pretty remarkable. We are going to spend 95% of the time talking about Petosemtamab, but I just want to draw your attention for a moment to the five molecules we brought into the clinic. Three have had outsized clinical activity. With zenocutuzumab, now branded as Bizengri, it is approved by the FDA for NRG1 fusion lung and NRG1 fusion pancreatic cancer after having received two breakthrough therapy designations. Our other molecule, MCLA-129, is an EGFR MET bispecific like amivantamab, and like amivantamab, it has very strong clinical activity in a number of different indications in lung cancer, and with Petosemtamab, we'll spend a lot of time talking, but it has really compelling clinical data to date in head and neck cancer and two breakthrough therapy designations from the FDA to really validate the importance of these clinical data with opportunity in colorectal cancer and beyond. We think it's a great place to be as a company, and we think 2025, 2026, and beyond hold tremendous promise for us. Great. Thanks for that overview. So, like you said, yes, we will most likely be spending 95% of this on petosemtamab. But, so I guess what I'd really like to start with is, you know, you recently received a breakthrough designation. And in your press release, there was an interesting sentence in there about that the FDA considered it with an updated data cut. And then in your earnings, you announced that the next update for the frontline combo is going to be in the first half. So I was wondering if you could tell us a little bit more about that interaction that led to the breakthrough designation, what that means for you guys, and then we'll get into the first half data cut. But I'm curious how that data cut played into that breakthrough designation. Breakthrough Therapy Designation is one of the tools the FDA has to help facilitate and speed the development of innovative new medicines. And specifically with Breakthrough Therapy Designation, as opposed to some of the other designations from the FDA, this really is the tool that the FDA has to identify drugs they believe have a real opportunity to provide meaningful benefit over currently available therapies. And it's almost always based on clinical data to date in virtually all of these assessments. So it's a really important metric that an independent pair of eyes, or many, many different eyes at the FDA, can look at a data set and say, "Wow, this seems really important." From our standpoint, Breakthrough Therapy Designation is very important because it allows our program, Petosemtamab, to have the attention of the most senior review teams and most senior staff at the FDA review division. It allows the FDA what's called regulatory flexibility. By way of example, we recently got Bizengri approved, our earlier asset, zenocutuzumab, in NRG1 fusion lung and pancreatic cancer. That was a remarkable approval, probably only able to get done because of the regulatory flexibility afforded by those breakthrough therapy designations, because it was pancreatic cancer in division three and lung cancer in division two at the FDA. It allowed for one data set to strongly support the approval of the second data set. Now here, with breakthrough therapy designation for Petosemtamab in both the first line setting and the second line setting, it allows us, or allows the Petosemtamab program, regulatory flexibility here as well in evaluating each of these data sets as the FDA considers the potential for accelerated approval or regular or traditional approval. So we think it strengthens the case and the opportunity for petosemtamab. Then lastly, for us as a sponsor, you know, we would otherwise, like all other sponsors, interact with the FDA in a very formal, very fixed manner. If it's a type A, a type B, or type C meeting, each of those have very specific mandated processes and timelines to engage with the FDA and then wait the 60 or 90 days and get a response. With breakthrough, it's not completely akin to, but it's much more similar to just picking up the phone and saying, "Hey, review team, what do you think about this issue?" Then across everything, right? Clinical data, safety data, the processes we approach, the ways we're analyzing our data, our process development, our manufacturing activities, all of these things, it allows us this really important flexibility in the way we can engage with the FDA. One other thing I want to comment on is it's really unusual for the FDA to provide breakthrough therapy designation for a combination. And the reason is because the FDA looks at the data and says, "Well, how do we know that your results aren't just outsized contribution from Keytruda alone?" When you have a combination, you don't really know. And all of you as investors have seen this movie before. Some single-arm oncology data set of combination therapy, like that should already have a whole bunch of red flags for you, shows a good result. And then, you know, later on in a registration trial, that result doesn't hold up. And so the fact that the FDA has reviewed our data and has monotherapy data to support it with Petosemtamab and saw a substantial enough signal above and beyond what patients could otherwise receive to give them confidence that, "Wow, this really can be a meaningful medicine," is, I think, a tremendous vote of confidence in the Petosemtamab program overall, and specifically Petosemtamab pembrolizumab or Petosemtamab Keytruda in the first line setting. I can't emphasize this enough about how virtually all other breakthrough therapy designations are either in the randomized setting or for a single drug itself. But the fact that we got breakthrough therapy designation for a combination is really important. So I'll come back to these two themes throughout the talk. Anytime you have only a combination data set in a single arm setting, you should worry about that. And you should challenge me and, frankly, any other company that only has a single data set of combination therapy, like, "How do you know?" So that's a really important theme. Okay, great. And thanks for that. It's not often that you can jazz up a room of 50 people about breakthrough designation, but you did. Can we move on to the first half update? I think what would be helpful is not only your expectations for where you think especially mPFS might end up, but what you think would be a good result, you know, even aside from predicting what you think Petosemtamab could achieve. There's been a lot of focus from all of you guys on median progression-free survival. And let me just challenge your thinking on this, that what we want to pay attention to is all of it, right? ORR, progression-free survival, and overall survival. We've guided, we'll have a clinical update the first half of this year. And I want you to pay attention to all of these facts and figures and numbers. The reality is that our registration trial, the primary efficacy endpoints are overall response rate and overall survival. We have to absolutely, absolutely win on those stat-sig and clinically meaningful difference above the control arm. So those two are really, really important. I don't want those to get lost as we talk about progression-free survival. So where's the bar is basically the question you're asking. There are two ways to look at this. I grew up in clinical drug development. So the first bar I worry about is what's the control arm going to be and how are we going to beat that? You all have to worry about larger questions. So while you worry about that, you worry about what's the competitive landscape too. So let me tackle both of these. On the approval side of things, Keytruda is the control arm in the registration trial. The overall response rate for Keytruda is 19%, or if you count the LEAP-010 trial, 25%. The median PFS is three months, and the median overall survival is 12.3 months or 17.9 if you count the LEAP-010 trial. That's it. Those are the bars for what we'll be compared to from an approval standpoint. And so far, we have a 67% response rate, and we didn't have enough follow-up durability, but already the vast majority of patients have passed that median three-month PFS. And it was way too early with the ASCO data set last year to tell you anything about survival. But all of those are important. On the commercial front, the competitive landscape has two competitors, zanzalintinib from Exelixis and ficerafusp from Bicara or BCA101. Both of those have some sort of data that provide other benchmarks along the way. Again, both of those analogs are combination single-arm oncology data sets. But the numbers there, the easiest number is a 9.8-month median PFS that's been cited by Bicara, which is a data point that we will be compared to. Importantly, as you see all of this data, you should also get to see the Kaplan-Meier curves, and then you can look at landmark rates of any of this along the way. Ultimately, all of these drugs have to win on survival. The first time you're going to know anything about survival is how many patients are alive at 12 months. The Keytruda rate is 50%-59% in these two studies. That's probably the, like, move all the chatter to the side, the thing that all these have to ultimately win on, that's it. So like, if you're only going to pay attention to one number, overall survival is the ultimate approval endpoint for these programs, all three of them. So that's ultimately where we have to win. When you say, you know, obviously we are focusing on MPFS right now, but when you say to consider all the data, what else will you be showing? And my specific question on that is, will you show landmark OS? So what I've said there is the landmark OS at 12 months is the first time you're going to be able to get a sense of the separation of curves. And I've also said anyone who wants to show you rates should show you the entire curve, right? So then you can draw your landmark anywhere, and you can sort of interpolate where you think the median is. You can see where the patients are censored. So you can get a sense of how fully baked the data is versus how much these additional patients might add wobble into the current estimate. But you should get all those data. That's what you should ask of any company presenting clinical data. Okay. And we had a pretty great discussion yesterday on our head and neck KOL panel regarding median OS. So I know you mentioned a couple of benchmarks there, but in thinking about where median OS could end up, you know, between that 12 to 17 range, where do you think you'd have to fall? Like, what do KOLs from your feedback consider a meaningful difference from pembrolizumab monotherapy? So I'm not quite sure how geeky to get into the numbers here. The first point I want to make is it has to be better than the control arm, where we've already put the control arm median at 12.3 months or 17.9 months, depending on which trial you look at. It's got to be better than that, both statistically significantly better and clinically meaningfully better. Nobody's going to be interested in a new medicine if that improvement is like, you know, a couple of weeks, right? Where does the sort of clinically meaningful bar lie? I think that's something you can ask the KOLs, but it has to be substantively better than those two benchmarks. I'll say the other thing I want to point out, and just for all of you to keep in mind, is we talk about medians, but actually the hazard ratio is calculated across the entire curve. So even if a median is better, but the whole curve isn't better, you could be fooled. So you just want to pay attention again to the whole curve of the survival curve. The easiest thing to talk about is the median, but it's the whole curve. Okay. And I think another key debate among investors, obviously, is this HPV positive inclusion. And so can you talk about, one, the percentage of patients that you expect to be HPV positive in both phase threes and how, relative to an HPV negative only trial, how that could influence outcomes? So in the realm of head and neck cancer, splitting out a subset of patients by HPV negative is a brand new thing. To take only the HPV negatives is a brand new thing. If you look at the prior registration trials in head and neck cancer, KEYNOTE-048 and LEAP-010 in the first line setting, CheckMate 141, KEYNOTE-040 in the second line setting, it's all patients. It's all comers, right? If you look at the INTERLINK trial, which was a failed attempt at registration, it's all comers. This relatively new idea to only carve out HPV negatives, that's a new thing by one particular company. But the point of view, the perspective historically of the field is, let's develop our drug in all the patients. And so we're following this very well-established path in developing our drug in all the patients. Our breakthrough therapy designation, when we provided our data to the FDA, both the breakthrough therapy in second line and the breakthrough therapy in the first line, is for all the patients, and showing clinical benefit in all the patients is really important. I will say, when the FDA takes a data set, they're going to look at all sorts of subsets, performance status zero versus one, CPS one to 19 versus 20 and greater, HPV positive versus negative. They'll look at all these subsets and look for tests of consistency across the subsets, but it really is historically the perspective of all the patients developing in the larger population. Generally, I think unless you're absolutely compelled to chop off part of your patient population, if you're not absolutely compelled to do it, it's a bad idea. You suddenly have a smaller population. You suddenly have less of an ability to rely on the previous data sets. You now need a diagnostic. You now need to go get a diagnostic approved by the Center for Devices and Radiological Health at the FDA for your clinical development. And then you end up needing a diagnostic test out in front of prescribing the drug for patients. It just complicates your life unless you're compelled to do it. And that's really why all of these other clinical development programs have really relied on, let's just test and develop in the overall population. How about briefly this, the notion that HPV positive patients might be smokers? Does it matter? So there is a KOL who has said, even as recently as yesterday, that smoking may change the responsiveness of head and neck cancer to cetuximab and EGFR antibodies. And I don't know his personal clinical anecdotal experience. He may have experience with one or two or a handful of patients who do that. But the statement is completely counter to the clinical data. Study after study after study, time and time and time again, when you take a population of head and neck cancer patients and treat them with cetuximab, you have zero responses. Even in data sets where the smoking rate is 77%, you have zero responses. It doesn't matter if it's the control arm, cetuximab only, of the INTERLINK trial, or the control arm, cetuximab only, of the afatinib trial, or the control arm, cetuximab only, of the MET inhibitor trial, or the ficlatuzumab cetuximab control arm in the INTERLINK trial. The response rate is zero. So I'm not sure why smoking continues to be an issue. It's just not supported by the data. I'm not sure how else to think about it other than to point to the data. Okay, great. And you know, we have about six minutes left. So I do want to ask some questions about the market and where patients are being allocated. And you know, I've had some investors express some concern recently about KEYNOTE-689 and adjuvant or neoadjuvant use of pembrolizumab. So can you tell us your thoughts on whether that could impact enrollment or the market in general for petosemtamab? So let me give a couple sentences of backstory here. KEYNOTE-689 was a study that Merck ran in patients with newly diagnosed local head and neck cancer. This is before the recurrent metastatic population that we treat. When patients are initially diagnosed, they get surgery, they get radiation therapy, sometimes they get a little bit of adjuvant chemotherapy. And Merck added Keytruda to the surgery part and said, let's give Keytruda before surgery, Keytruda after surgery, let's see if patients do better. And lo and behold, patients' event-free survival, meaning how long it takes for them to have a recurrence, was much lower if they got the Keytruda thing around their surgery. And the question has come up, wow, all these patients are getting Keytruda early on, is that going to mess up your population of patients in the marketplace? We think the impact will be minimal at best. And let me walk you through why. If you look at all the patients with newly diagnosed head and neck cancer, the surgery part, patients who go to surgery, is only about a third of the whole set. And already surgery alone cures two-thirds of those. So you're only left with about a third of a third being the patients who have surgically resectable disease who then have a recurrence. So only about a tenth, one out of ten patients, roughly, are in this small population that ends up going forward. And if you have, you know, use of this Keytruda regimen, in half of those, it could impact, you know, some patients who could otherwise go on to a Keytruda-based regimen in the first line setting. But the reality in oncology is, like, these patients don't have many other good options. If Dr. Tara, your patient comes to you six months later after surgery, after having gotten Keytruda, and says, wow, I have a recurrence, you know, what are your options to give that patient? cetuximab chemo? Typically in oncology, and it's a little bit more complicated in the IO space, but certainly with chemotherapy, if a patient has a six-month drug-free interval, you tend to use the same drug again, or you can use the same drug again. And so even on those patients, that 10%, who maybe some of them have an impact, but then they recur, we think it's going to be a really small fraction, if at all, who are impacted by this in the overall marketplace. Okay, great. And then briefly on the second line, I think what would be helpful is getting your understanding of how many patients are going to funnel through from the front line to the second line and receive an EGFR-based therapy like Petosemtamab, and then separately whether both or one of the EGFR inhibitors in the front line are going to be approved. Could you give them sequentially? So there's sort of two questions embedded in here. One is how many patients would really flow through to be able to get an EGFR-based drug in the second line setting. And you know, surprisingly, even Keytruda, which has the best data of any drug right now in head and neck cancer, is not used 100% in the first line setting. There are a lot of patients who flow through and don't get it in the first line setting, right? And when we did the math, it was sort of a no-brainer to run a registration trial in that setting. The second point is, could patients get an EGFR inhibitor after an EGFR inhibitor? And again, you know, it depends probably on the disease context. I would imagine, and this is my opinion, so you should actually talk to a real head and neck cancer doctor, not someone who's trying to channel one here. I would imagine that if a patient gets an EGFR-based antibody and progresses through the whole treatment, you're probably not going to try that again. If on the other hand, a patient gets an EGFR-based antibody, has a dramatic response, has a drug-free holiday of some period of time, quite reasonable to think about that again. So it depends a lot on the dynamic. Okay, great. So I know I lied to you and we spent 99% of the time on Petosemtamab, but I do think, you know, there's a lot of meaningful activity in the pipeline with CRC, with this Biohaven agreement that you guys announced. And so I think what I'd like to do is toss that to you and say what is the most underappreciated, either you could talk about Petosemtamab still or about the pipeline that we haven't yet discussed. So the most underappreciated thing, you guys will be surprised to hear me say this, but I actually think it's Petosemtamab. And what's not appreciated is the strength of the clinical data for Petosemtamab. It's not only in combination, but monotherapy, not only first line, but second line, not only the overall population, but individual subsets, and every single efficacy endpoint. And the gap between the robustness of this data compared to, which is incredibly solid, compared to other molecules we talk about in this space, which each have, you know, 20-30 patients' worth of single-arm combination oncology data, it's just like, it's dramatic. And the gap between our drug and where the control arm therapy is on these registrational trials is also really dramatic. And as evidence of this, the FDA granting two breakthrough therapy designations to Petosemtamab really underscores my belief that this is a compelling story. I've been in clinical drug development for more decades than I care to confess, and this is the best oncology data set I've ever had. This is a remarkably strong data set across the board. And as a company, it's incredibly important to me that we execute effectively. I can't stress this enough. Companies find all sorts of ways to screw up. Our ability to bring zeno from getting rejected early on in an NRG1 fusion context to getting FDA approval in NRG1 fusion lung and pancreas cancer, our ability to start to make it through Project Optimus and get our dose selected very efficiently, our ability to start phase three registration trials last year, our ability to have tremendous uptake in these trials early on, I mean, you're welcome to look at ClinicalTrials.gov for countries and territories and sites active. Our ability to execute on this, our ability to provide the guidance of substantially enrolled by the end of this year is all incredibly important in making sure that we don't screw this up, that we really make our commitment to the broader stakeholder community, but important to patients, and get this drug on the pharmacy shelf in the most efficient and effective way we can, because it matters. This is really why we do this. Okay, great. And with that, we are out of time. But Bill, thank you very much for your time. And thanks everyone for listening.