Okay. Excellent. Great. Thank you, everyone, for joining us, joining our fireside chat with Coherus. I'm David Allemann, one of the biotech planners here at UBS. It's our great pleasure to have Denny Lanfear, Chief Executive Officer, and Theresa LaVallee, Chief Scientific and Development Officer. Thank you for joining us. Before we start, I just want to, you know, quickly say that for just logistics for anybody who are in the room, if you have a question, please you can scan the QR code on the screen if they pop the screen here, and then you can ask a question, and it will show up on my iPad here. So, you know, feel free to ask away, you know, any questions you have, and I'll be happy to ask the question here for the management team to answer. All right? With that out of the way, Denny, Theresa, welcome. Thank you, David, and thank you for the invitation to be at UBS today. Yeah. Thank you. Great to have you here. To start things off, maybe you can quickly give us a high-level overview of Coherus, some of your pipeline programs and also your overall strategy. Sure. First of all, let me say that Q3 was the first quarter in which we were solely an innovative oncology company, having finished the divestiture of our similar business in Q2. We are very excited. We had a very good quarter. We have considerable momentum now going into the end of the year and into next year, particularly with respect to the patient accrual with our clinical studies. As you know, we have studies across more than half a dozen indications with our CCR8 molecule, CHS-114. We have a study that is launched and doing very well with Casdozokitug, again, liver. We are spooling up another study with a cooperative group in lung. All of the sites are enrolling and at full bore. We are pretty fired up. We find that the investigators are very interested in the mechanism of action of our products and how they might help the patients. Our team has been going and talking to the investigators, and they find that they're really very enthusiastic to put patients on the study and see how they work because these are really significant breakthrough therapies. I think that Coherus presents a very unique value proposition in the oncology space for investors. We have excellent products. Our products, you know, for example, our PD-1, Toripalimab, is next-generation PD-1, has very unique binding sites to the FG loop, demonstrate activity in low PD-L1 states. The lens that we view Toripalimab, LOQTORZI, through is one of both a revenue generator in nasopharyngeal cancer, but also a revenue multiplier because we're combining it with both our key assets in the pipeline. I'll talk in a little bit about how we're also combining it with others. You know, we're very, very open about doing combinations, and we feel that combinations of therapies are the way that we're really going to move the bar with respect to patient survival. Theresa will say something about the various combinations that we're contemplating in, you know, a number of therapeutic areas later. Back to the drugs for just a moment. You know, we have a next-generation PD-1 that's doing well. Secondarily, we have a CCR8, which we think is best in class. Theresa talked to you a little bit about it, but 114 is highly selective. When that molecule was brought forward, it was screened against over 5,000 other proteins on the surface of cells in your body, and it only reacts to CCR8. This is the reason why it's so highly selective. Of course, we have some excellent data that we produced in patients, some biomarker data, which we have presented. Casdozokitug is, I think, a very interesting molecule also. It's an anti-IL-27. As it turns out, IL-27 plays a very key role in immune system homeostasis upon pathogen invasion. This happens, for example, in barrier tissues in liver and in lung. It has shown really strong efficacy in lung. In a particular study on a background of atezo-bev, which is standard of care, it showed, for example, a 17% complete response rate, which I think compares quite favorably with the 8% of standard of care. We are going on and we're doing a follow-on study at two doses on that also. The second key thing about the company, I think, that is unusual with the value proposition is the data catalyst. We're gonna come forward in mid-2026, all these studies. For example, with CHS-114, we have studies that are underway in gastric cancer, esophageal, colorectal with metastases, colorectal without metastases, and of course, head and neck. It is a very, very growing, vibrant field. You know, as you know, the Nobel Prize was just awarded for the scientists who moved this forward recently. Casdozokitug will turn over some data cards next year in liver, two doses, I said again, with atezo, with Toripalimab. That is exciting. I'll talk a little bit in my closing remarks about some of the deals, which is, I think, the third very, very interesting part of the company's value proposition. Deals are important to us because unusually for a company at our state, we have global rights to these products. We haven't sold these rights off. We have the opportunity now to develop all this data in phase two, going into pivotal studies and to do both U.S. deals and ex-U.S. deals with these products. Ex-U.S., particularly in some Asian countries. Liver cancer, as you know, is a big issue, hepatocellular carcinoma. We look forward to getting partners in Asia for Casdozokitug, but also for CHS-114. We think there's the opportunity to do a number of things there. I'll just stop there. I think for a company of our size, we have a lot going for us. You know, we put together some very strong deals over the past year, divesting the biosimilar business. We reported $198 million in cash on the balance sheet at the end of Q3. We're very strong with our financial and our fiscal management and our operations. We look forward to turning over the data cards, as we go forward. That's great. Thanks, Denye. It's very exciting. You know, especially coming into next year, we're gonna get a lot of updates and potentially, you know, probably hear a little more on the deals front too. Very excited to see what's happening next, you know, 12 - 18 months. Now, let's talk specifically about some of the programs here. The first one, of course, is LOQTORZI, Toripalimab, as mentioned. It's now approved for front and, you know, front and second line nasopharyngeal carcinoma. You mentioned a little bit about there's some differentiation of this drug versus other anti-PD-1s such as binding site, affinity, compatibility. If you can just tell us about some of the things you're doing to expand that, you know, some of the combination strategies you're planning, you know, for Toripalimab. I'll let Theresa take that. Theresa, you wanna talk a little bit about where we're using Toripalimab in conjunction with other therapeutics? Yeah. Thank you. As you said, it's a next-generation PD-1 based on its increased potency, unique epitope, and differentiated clinical activity in phase three studies showing similar activity in both when in combination with chemotherapy and PD-L1 high and PD-L1 low. PD-1s are foundational, a standard of care. Advancing treatment in combinations requires a PD-1. The head-to-head studies go against standard of care, which is a PD-1. You wanna make sure your combination with a PD-1 inhibitor at least starts toe-to-toe. If it's a little bit better, then your probability of success and your hazard ratio is higher. We really see moving the field forward and treatments for patients in combinations with our own pipeline, which we'll talk about, I think, in more detail and the excitement of the data there. Also now with working with other biotechs because we're nimble, we're fast, we have a prioritized program in Toripalimab. We've announced a couple of collaborations where other people are using their unique mechanisms of action, their clinical data to advance tori in tumor types that are important to us, such as head and neck, lung, liver. It really complements our own development and continues to build out the awareness and the use in the U.S., which also helps our commercial team. We think overall, looking at these combination strategies and continuing to gather data and advance Toripalimab in development as well as look to get it to other indications on the market is a really important approach for us. Got it. Great. And, and so then let's talk about the nasopharyngeal carcinoma. You know, LOQTORZI is approved in 2023. You have seen a few quarters of, you know, of revenue so far. And in the most recent quarter, you got about $11 million, you know, up 12% quarter over quarter from $10 million last quarter. You know, how has, you know, can you just talk a little bit more about how has the, the adoption been so far across different segments, including academic settings as well as community settings? The first appointment I would make is that, LOQTORZI really has real outstanding efficacy, in this disease state, near nasopharyngeal cancer, really, really strong hazard ratio and, you know, further, extends, you know, survival out from like 22 months, well, well past, 48 months and so forth. When you talk to physicians about the data and you show them the data and the studies, and by the way, there isn't another PD-1 that has this sort of data, in the U.S. When you, when you do that and you talk to them, the, the physicians are converted, right? They're, they become, you know, Toripalimab users in this disease state. What we have seen them doing is use Toripalimab when their additional NPC patients show up. We launched this product, in Q1 2024. We're in the second year of launch. Now, Q2 over Q1, we saw about a 36%-37% increase in sales. A big chunk of that was inventory build because inventory had been depleted. But about 20% or so of that was actual pull-through increase in demand Q2 over Q1. So that's a pretty good clip. Now what we saw last quarter, Q3, you know, over Q2, we saw three of our four regions, and I would say we have four regions in the United States. Three out of four regions did 21% average growth, which is really, really good. We had one region that was lagging. It was flat, pulled everyone else down. But, that being said, I think we were pleased with those results. If we do 10%-15% revenue growth, you know, from here somewhere out in the middle of sort of 2028, we get to our target of $150 million-$200 million. However, we wanna make sure that we get these folks. And there's actually two segments of the Toripalimab market, which are important. The first are the academics who are very cognizant of and observing of the NCCN guidelines. So we are the only first-line preferred treatment with Nasopharyngeal, very strong NCCN positioning. Now, these physicians are more specialists. So they're, they're up to speed in the literature. They know exactly what's working and so on. So they're early adopters, and we've seen very good progress there. But another significant part of the physician population is the community physicians. And they treat a wide variety of cancers. They treat everything that comes in the door. They only see a nasopharyngeal patient like, you know, one or two, you know, years. That is a higher bar because those physicians are sort of just not cognizant that Toripalimab is on the market, that this is really an outstanding therapy and it is what they should use with their patients. When we get to those doctors, they understand, they start writing scripts. I think we needed some additional, a couple additional things really to get to these community physicians and make sure that these patients get treated. We added some additional headcount across there. We also have some virtual sales reps that are going, and we have also done some additional things with our electronic efforts. We feel confident that we'll get on the escalator with this, you know, into next year, and this will be a very nice growth rate for the product. Overall, it's really just a function that it's a very rare disease in the community guys. They just don't see it that often. Got it. Yeah. That's really good. And then just in terms of the label expansion strategies, as you know, Theresa, you mentioned about the combo strategies that you combine, you're thinking about, what can you help us understand what are some of the label expansion, you know, strategies you're thinking about going forward? Yeah. I think as we talk about the pipeline, we can look to the different indications that we're evaluating to get additional. The important thing there is that it's a two-for-one strategy, right? We invest in the pipeline, but when we get CHS-114 or Casdozokitug approved, we also get Toripalimab. When we looked at what it would take to take the positive phase three studies and like Toripalimab was just featured at the presidential session at ESMO with the combination with the ADC in bladder cancer, you know, standing ovation with the PFS curves. It just continues to deliver. Those data are beautiful. To bring that to the U.S. as a China-only study, it would be a couple hundred patients in a couple years. We feel like it's better to keep advancing beyond the data sets that are here today. It gives us continued confidence in the molecule seeing data like that in New England Journal of Medicine article. Label expansion with the pipeline and others. Got it. Okay. That's, that's really helpful. Great. Moving on to, you know, your second program, which is the 114 and the anti-CCR8 program. Tell me, tell us a little bit about that program. You know, very interesting mechanism of action because you're targeting CCR8 Treg. And apparently the scientists who discovered this, this pathway was recently awarded Nobel Prize for that, right? So, you know, just describe a little bit more about the target, you know, what makes it so compelling? I'll give you the sort of the high-level flyby now. I'll let Dr. LaVallee, you know, backfill a little more science. I think that it's really significant that the whole Treg field has now moved to the fore at this point, right? There's a number of teams, as you point out, that are working on Tregs. And Tregs, you know, over the past 20 years, they have, you know, it's become very clear that Tregs play a significant role with the immune system, you know, in cancer and so on. A lot of people have hoped that if Tregs, particularly in the tumor microenvironment, were depleted, then what would happen next is the infiltration of CD8 positive T cells. You would remodel the tumor microenvironment. This was a long, long-held hope. I think the Nobel Prize fundamentally underlies the scientific impact of this and its potential therapeutic potential across these. What I like best about, you know, the Tregs in the space and Treg depleters is it's highly targeted. You can go after cancers where there's a high percent of the Tregs present are CD8 positive or CCR8 positive. You can also go where there's a lot of these, high density. The clinical program is one of exploring just what happens when you deplete, you know, across these various cancers. There are many cancers. There's the entire GI tract here, esophageal, gastric, colorectal. There's pancreatic, prostate. There's a plethora of cancers that are so-called cold where they are not immune responsive. This is the promise of this. What is very interesting about CHS-114 is that it is such a highly selective molecule. As I indicated before, when it was screened, it was screened against over 5,000 different cell surface proteins. It only engaged with CCR8. I think this is going to be an important differentiator because a lot of the other teams we know have molecules that react not only just against CCR8, but, you know, elsewhere in the body. You end up with, you know, GI tox or skin tox or whatever, those types of things. Having a very, very high-quality molecule, I think, is going to be a significant difference. You know, having this sort of highly targeted therapy where you know where to go with the rifle shot, I think is very important. Maybe Theresa, you wanna add a little bit about the clinical product selection and the MOA? Yeah. Maybe just taking a step back for why we're so excited about the T regulatory cells getting recognized for the Nobel Prize. You know, we were surprised and thrilled to see that happen. I actually worked with Fred Ramstill at the Parker Institute and found it hysterical that he was off the grid camping, which is so typical in Laura to get the call and be like, "Fred, get..." You know, so it tells you how much we didn't, as a group, think that it would be recognized. I think it's the right time and it's consistent with how the Nobel Committee has really tried to focus on emerging areas of science that are really important. Clearly, like Alexander Rudensky is another forefather of Tregs, but consistent with how the Nobel's awarded to first discovery, went with Fred and Sakaguchi. The idea of T regulatory cells really holding down peripheral immune tolerance. If you deplete them, you get rid of that. Fred and Sasha are also involved in a company to treat with Tregs to dampen autoimmunity since tumors exploit this to turn off the immune system and resistance to therapy broadly, chemotherapy, radiation, and of course, PD-1, right? Everybody's known this forever, but how do you get rid of Tregs only in the tumor and not cause terrible toxicity to the patient? 'Cause we know we need Tregs for peripheral tolerance. CCR8 is the answer. What was really missing is a way to just get in there and selectively target Tregs in the tumor, removing the immune suppressant and really opening it up now as you take the resistance mechanism away to potentiate therapy broadly. Our clinical program is really designed to evaluate, since it's a targeted therapy, where's the target highest? Also, in what context? The studies that we're doing with the different tumor types are very strategic and designed to inform us how to move forward to bring immunotherapy within PD-1 approved indications like head and neck, gastric, esophageal, but also tumor types that have really been underserved. I mean, we see Tregs in a lot of breast cancers. We see it in colorectal cancer, MSS CRC. I think there's a large opportunity here for CHS-114 across solid tumors. Got it. Can you just help us understand some of the, you know, clinical data you've generated in head and neck cancer so far? Yeah. I think, you know, in early phase development, you wanna know, does your drug do what it said it would do? And do you get the exposure you want? And do you have the safety profile? We've answered those questions resoundingly. Yes. Hits the target, tickles the target, has the safety profile to do combinations. The thing that's surprising, which usually you get surprised in like, oh, it's gonna be harder. We got a surprise that as we took the Tregs out of the tumor after treatment of CHS-114, this large infiltration of CD8 T cells, which we know is essential for immunotherapy to work. What's been the limitation for T cell engagers in solid tumors? There's no T cells in the tumor for them to activate. You know, they bind the tumor, then they gotta tickle the T cell. If it isn't there, CAR-Ts, phenomenal in hem malignancies. How do they get into the tumor? Treatment with CHS-114 and these types of treatments can really lead that. We've shown that. We've shown that we have the right dose. We have immune activation. We've done exactly what we said without causing terrible autoimmunity. We've seen early signs of response with, in combination with Toripalimab. Now it's about delivering data in 2026. Where do we see that efficacy signal that we can take it quickly in development? Yeah. That's helpful. On that front, you know, you have four indications that plan to go into, right? As you mentioned, head and neck, gastric, esophageal, CRC. You know, which one is most exciting to you? Or do you have a favorite child? I think it's really important that this clinical development plan is purposeful and thoughtful. I think that we've seen activity in head and neck. We know that there's a treatment approach that could affect disease. The question is, does Toripalimab and CHS-114 in the second line head and neck setting reverse PD-1 resistance at benchmarks that are currently being shown with novel agents? EGFR, bispecifics, ADCs are hitting high ORR and duration. We have to be competitive in that space. We're hopeful, but the data will show us if we have sufficient activity to be competitive in second line head and neck. What we started with when Denny was talking about the targeted therapy, I mean, I'll use two analogies of how you need to learn early in development. PETO, Merus's compound, shockingly good data in head and neck, right? The target was identified in CRC. That was the tumor type where the LGR5, EGFR, bispecific was gonna knock it out of the water. Head and neck did. CRC's showing some activity, not as good, right? They've learned something about the biology. The BRAF MEK inhibitors, you know, when they went in, you just go and treat RAF mutated, RAS mutated tumors, right? They have a label across solid tumors except for colorectal. We learned that that's because of EGFR. Breakwater this year got that phenomenal data and got approval now in colorectal. Some of it is about learning. It did, it's not that it didn't work in colorectal. It's just that it needed something else, right? Our study is designed to learn. Is it the density of CCR8 positive? Is it just that? Is it the ratio of Tregs to CD8s? Also, looking in tumor types like colorectal cancer where there's a lot of biology and no approved PD-1, is that the right context given the biology there? I think what we want to learn next year is what are the efficacy marks we're hitting, what's the dose, what's the safety profile, and what's the fastest development to advance this molecule. The one, I think I will like all of them that show activity. The one that I will love next year is the one that gets me to market fast. Yeah. I agree. I think that the, you know, the promise is very broad, with the whole CCR8, Treg, depleter class. You know, certainly in other people's hands, there's been excellent data in gastric. There's, you know, been very good data in PANC and a number of things. So I think that overall, as Theresa said, we have a broad yet focused program. We've placed bets. The nice thing is, there's very strong mechanistic justification for investigating where we're going. We'll just have to turn over the data cards and see how that turns out. In all these places, especially places like head and neck where others are moving forward, CHS-114 also has the potential not just to compete, but to be complimentary as an additional orthogonal mechanism of action. You know. Very important. Those drugs do not deplete Treg cells. And Treg cells are a problem there. You know, you can go head to head and so on. We are also getting, you know, and back to the deals for a moment, we also get good interest from companies who talk to us about potentially combining our CCR8, CHS-114 with their other products in these indications. That is a win for us too. I would just say as a small company, we are, you know, we are sort of uniquely positioned. You know, we do not have an axe to grind where we have to stay just in our own space like some of these big shops, right? In the first instance, we are a small biotech. Any success, you know, broadly with the mechanism of action and the products will be disproportionately beneficial for Coherus, right? We'll get, we'll get banger for a buck than if one of the big giant, you know, pharmas. Go ahead. The second thing is we're free to do deals and combine with others. You know, you know, Theresa has a lot of very close ties throughout the scientific community and a lot of big companies. And, you know, we're very open-minded and we really wanna benefit the patients. We wanna provide that step change in patient survival. We're okay if they take CHS-114 and combine it with a bispecific or an ADC or radiation therapies. We're fine with that. That, that's a, that's a win-win. Anything that gets you there. And so that, that's the kind of things that we look at. For example, we were talking about collaborations within the United States. It's just like the collaborations that we do with Toripalimab. We'll just give them Toripalimab, put it in your studies, and when they get approved, we get approved, we get a label claim. So, you know, we think the rising tide floats all boats, and we think it's a unique strategy. But one, you know, our company being what it is, we're able to embrace. Got it. Got it. That's helpful. Great. And then just this last question on, on 114. And, you know, we've seen a few different competitors from big pharma also developing CCR8 target. Can you just tell them more about your, you know, 114 differentiation compared to other, you know, CCR8, you know, competitors out there? Yeah. It's a good question. We're learning about these, and Denny's mentioned a couple of times. Selectivity matters. We know off-target binding can have liabilities, particularly toxicity. We have heard chatter from a few folks. We were just at SITC, and maybe some of the programs in the big pharma shops are shelving their programs because they've hit toxicity. We know that ours is selective. We have an acceptable safety profile with the data we have to date. We also have potency, both from where it binds. It's in the picomolar range from an affinity, but it's ADCC enhanced. Not all of the programs out there are ADCC enhanced. Shionogi showed data at ASCO this year with responses, CR and MSS CRC. Whoa. Nice, right? They're a wild type IgG1, not as potent as ADCC enhanced. and then there's the differences, you know, do you bind to compete with the ligand? We think it's better not to compete with the ligand because, it's competition. So you don't get as much binding. And this is a bind and kill mechanism. That's also important because ligand blocking, you kill the cell. It's not gonna signal. So dead cells don't signal. and then clinically, we're gonna differentiate through the combinations, through the approaches. We think adding it with Tori, we feel very, confident and excited that we can compete and, and deliver data and continue to be the one showing data. We are the first to show CD8 infiltration in the tumors. Shionogi's the second. No one else has shown that yet. Yeah. I think in 2020, just to dovetail on Theresa's remarks, I think in, David, in 2025, Coherus Oncology demonstrated significant leadership in this field. We were the first one that showed depletion, then the attendant infiltration, CD8 positive T cells, and so on. You know, the SITC webinar, which just occurred two weeks ago, was the most highly attended. Now we have the Nobel Prize. You will see us, in 2026, continue to press forward with our scientific leadership, being in panels, going to meetings, and moving the field forward for the benefit of patients. I think that's very important. Again, as a very high science small company, it's something that we'd love to do. Got it. Great. We have about three minutes left. I just wanted to kind of, you know, touch base really quickly on Casdozokitug, your third program. So I'm just curious around the data expectation in first half 2026. Can you maybe assess some expectations around what kind of data we should be, you know, expecting? With respect to the hepatic cellular carcinoma data? Yeah. Theresa, you wanna just chat about that? Yeah. So clearly you've mentioned the activity we've seen in the initial phase two showing improved depth of response, improvement in ORR, improvement in PFS on top of standard of care. Now we have the randomized study with Tori Bev. We wanna see that safety. We wanna see that improvement. Initial data, we need activity equivalent to. It takes time for it to mature to see that depth and improvement in ORR. That's what we'll be looking for. That would be a dataset that would really set us up to then design a phase two, three, and have all the appropriate health authority conversations. A second dataset that shows that profound depth of response and improvement and duration would be enough to advance development. Got it. Now, how quickly do you think you can actually move into a phase three trial? You know, it's the usual metrics, right? Get the data, put the packages together, have the conversation. So half a year. Got it. Very, very exciting there. I think that's a very interesting molecule and a very integrated indication. Hepatocellular carcinoma is a $4 billion space in the United States. We've shown phenomenal efficacy. We have a lot of folks interested actually with us in that molecule. It's first in class, which I think is also very remarkable. IL-27 plays a fundamental role, as I talked about, with respect to, you know, pathogen infiltration into barrier proteins. The biology, the translational aspect of the biology really holds water. I think that's why it's doing well. Got it. Great. And just lastly, Denny, you mentioned about some of the BD deals you're planning to do, and, you know, some of the key catalysts over the next, you know, 12, 18 months. Maybe just highlight, you know, more what kind of things we should be watching for over the next 18 months. I think we've demonstrated the ability to do outside deals, particularly with our divestitures and a number of other things. You know, our acquisitions have been low. Our divestitures have been high. We have a really extraordinary portfolio here at these two assets. We have global rights to both these assets. That is really important. There are a lot of flavors that we can do, certainly XUS deals. I think the key thing with deals is they, first of all, validate the value of the assets in the eyes of big pharma or the other partner. They bring in upfronts to offset, you know, the clinical costs. Lastly, they set us up for cost sharing for pivotal trials later on. I think that is very good. We have a lot of latitude with the deals. For example, as I said, you know, we can do not just XU.S. deals, but we're very happy, for example, to take CHS-114 and put it in the hands of other people to mutually advance their products, you know, which I think is mutually beneficial. We'll do those sorts of things too. Stay tuned. As the data rolls out, six, 12, you know, 18 months, you'll see us go chase those things down. Great. We're looking forward to exciting 12-18 months. Thanks. Yeah. Great. Good so far. Great. I think with that, we're out of time. Thank you, Denny. Thank you, Theresa. Thanks, David. Thanks UBS for having us. Thank you.