It is now my pleasure to introduce Dennis Lanfear, CEO of Coherus Oncology. Thank you. Thank you to the organizers for the opportunity to talk to you about Coherus Oncology, an emerging innovative oncology company based in the Bay Area in Northern California. Let me first apprise you of the company's forward-looking statements and direct you to the requisite SEC filings with respect to our products. Today I'll talk to you about a few things. First of all, the value proposition the company presents, which I summarize as drugs, data, and deals. I'll talk to you a little bit about LOQTORZI, our foundational PD-1 and next-generation product that we have on the market. What's really interesting, though, today, what I'll talk to you about is CHS-114. CHS-114 is a highly selective Treg depleter, and Treg depletion is a very important emerging therapeutic approach, as recognized by a recent Nobel Prize. I'll also talk to you about our other pipeline asset, casdozokitug. This is an anti-IL-27 brought forth by Chris Hunter, University of Pennsylvania. We're developing this asset in liver and lung, and I have some very positive data to show you with respect to those studies. Lastly, I'll talk to you a little bit about the global rights for these products. Now, regarding the drugs and data and deals, as I said, casdozokitug is being developed in liver and lung, but LOQTORZI is developed in nasopharyngeal cancer where it is approved. We have a number of studies ongoing with the pipeline in 2025 and 2026. As you can see, we expect to turn over these data cards by mid-2026, particularly with respect to head and neck cancer and further on with liver cancer with casdozokitug. Two other important studies are also underway: colorectal studies with CHS-114 and gastric. Regarding deals, Coherus Oncology has a very strong track record of deals with both the divestiture of its biosimilar assets, but also a number of opportunities are underway combining our assets with others' pipelines that I'll talk to you about in just a moment. Here's our pipeline. The first point that I will make to you is that LOQTORZI is both a revenue generator for the company with respect to nasopharyngeal cancer, something I'll discuss with you for just a moment, but also a revenue multiplier. This is a very, very active next-generation PD-1, and we combine it with both of the assets that are in our pipeline. Further on, when these get approved, then we will have two products approved, and we will have expansion of the label for the products. Here you can see a number of our products that are under development now, and you can see the colorectal cancer, which we've just recently gotten underway. We'll see data from colorectal cancer with CHS-114 in the second half of 2026. Head and neck cancer is underway. That will roll out probably in the first half of 2026, perhaps around mid-year. And then other GI cancers. I'll talk to you a moment about how important our approach to GI cancers is. These are large and growing problems, as just outlined, I think, and underlined by the JAMA publication. Now, with respect to casdozokitug, ACC liver cancer, I'll talk to you about that data in just a moment, and I think what's particularly interesting there is some of the complete responses that we've seen. I won't talk to you today too much about squamous, but this is an area where there have been monotherapy responses, and it's very promising. We're going to get a study underway in 2026, and you'll see data there, as you see here, in 2027. This combined pipeline addresses about $30 billion in opportunity in the U.S. alone, across a number of these indications, about a half dozen indications for each of these products in consideration. As I indicated to you, LOQTORZI is a revenue multiplier. I'm going to talk to you next about how this is a next-generation asset brought forward with really astounding science. Partnered indications also. One of the things that we do with LOQTORZI is we put it in the hands of other people who are developing complementary assets that are not included in our own pipeline. They do that at their own expense. We simply provide the drug. When those assets are then approved, we too will also have an additional indication. One of the things I'll talk to you about at the end of the presentation is the significant ex-U.S. opportunity. Our pipeline assets, we have full global rights to. This allows us really to both do licensing arrangements within the U.S., but also ex-U.S. What that will do really is help us with respect to the further-on registration studies. Now, let me talk to you a little bit about LOQTORZI. LOQTORZI was brought forward by Lieping Chen, a very prominent scientist who first discovered the PD-L1/PD-L1 interaction. Lieping Chen's idea was that you would not just bind and occupy PD-1 so it could not bind to PD-L1, but you would do so at the FG loop. FG loop binding, and with high affinity, does something very interesting. It results in the internalization off the surface of the T cell of the PD-1 receptor and subsequent very positive and differentiated impact on what's called SHP-2 signaling within the T cell. When we first brought LOQTORZI on board, we didn't really understand why this occurred. It was the highest performing PD-1 of all those that we screened. Now we know. This has been demonstrated clinically. Here you see the LOQTORZI data in esophageal cancer, and you can see very similar hazard ratios and responses in both low PD-L1 and high PD-L1 states. However, here is Keytruda, and you can see there's a significant difference. These molecules do not work in low PD-L1 states, generally speaking. As a matter of fact, nevo, pembro, tizi, all these molecules have a very difficult time in low PD-L1 states. It is remarkable that Toripalimab has been approved in Europe for low PD-L1 esophageal cancer. This is a snapshot then of where we are with the market. We launched this product in early 2024. We're clipping along very nicely. Last couple of quarters, we're doing 10%-15% growth, which we'll see both in terms of the revenues and in terms of the pull-through, the number of units. We expect to have this market fully saturated by mid-2028 and approach the midpoint of the $150-$200 million range. Importantly, this is the only NCCN-preferred category one IO treatment for this cancer. This really is a very strong educational point with the healthcare providers when our team talks to them. There's about 2,000 patients out here, and we're well on our way. During 2026, you will see a further increase in the penetration in this particular market as we get broader and deeper coverage into nasopharyngeal cancer. Now, let me talk about casdozokitug, which is very, very interesting. I'll stop just a moment on this slide because I think it's very important. The Nobel Prize has now recognized the potential, the therapeutic impact of T regulatory cells. This is a long time coming. As you can see, things got started in 1995 when Sakaguchi actually discovered Treg cells. The seminal event, though, really happened in 2016. In 2016, Rudensky, who is Chairman of Immunology, Memorial Sloan Kettering, discovered that there was a surface protein on these T regulatory cells called CCR8 only in the tumor microenvironment. You have the tumor, you have the tumor microenvironment, it's encapsulated, and the Treg cells that are inside this particular area have this marker. The supposition was then that if you were able to selectively bind CCR8 and remove those Treg cells, you could then get subsequent infiltration of CD8-positive T cells and a positive response in tumors, in cancer tumors. Here's what Tregs do. Basically, they moderate the immune response within the tumor microenvironment. Here you see in this little cartoon, removing them, as I just elucidated to you, would have thought to then release the immune system to attack these tumors. This is a problem across a vast number of tumors, which are determined or called cold. That means they are not immune responsive. They are here liver, colorectal, basically a lot of these GI cancers are this way. This is a huge problem, 70% of these cancers. What happens is that the Treg cells get into the tumor microenvironment, and it results in T cell exhaustion, no T cells within there. Now, what's very interesting, if you take a look at all of these various cancers, you can develop a very targeted approach. In the left panel here, what you see are two things. That is the density of Tregs, right? How many Tregs there are per volume, and then what the percent of those Tregs that are there are actually positive for CCR8. You could see some of these cancers, for example, like gastric and head and neck, they're high upper right quadrant, that's very favorable. But also a number of teams, as you see on the left panel here, on the right panel, I should say, there's been very positive responses, partial responses, complete responses across a number of these tumors. Here you have pancreatic tumor, very underserved, very tragic tumor. Colorectal cancer, first-line therapy for colorectal cancer is chemotherapy. So there is a number of these that we can pursue, and I will show you then in our own program how we're going after these. But first, let me talk a little bit and take a step back and talk about the biology of CCR8s and why our molecule, Tegmote Kitug, known as CHS-114, is so important and why this is differentiated. So this is a very important slide. On the far left, as I just talked about a moment ago, Rudensky discovered that this GPCR receptor, CCR8, was on the surface of the Tregs that are in the tumor microenvironment. Okay? These GPCR receptors present very little real estate to bind to for monoclonal antibodies. Selectivity is very, very important. What you see here then in the middle panel is the selection process that was undertaken to develop CHS-114. CHS-114, over a long period of time, at the direction of Dr. Rudensky, was screened against 5,280 different cell surface proteins in the proteome. This is really remarkable. During the time that this product was put forward, a lot of effort went into making this right and making this best. You can see that CHS-114 alone binds just to the CCR8 in these cells. We have also looked at a number of competitor proteins, and you see these competitor proteins here in the right panel, Bristol-Myers Squibb, AbbVie, Roche, and so forth. We have made those molecules, and I offer a couple of them here just to show some of the off-target binding that is there. For example, competitor one binds competitor two J chain. J chain is very important in terms of gut. It is in gut, a lot of gut tox. This particular competitor now is seeing gut tox, okay? And on and on, and with skin tox and so forth. This is something that was sort of thought about beforehand that we really focused on quite a bit. I think what's going to happen as this whole field moves forward, those that have had highly selective molecules will do better, particularly when they address some of the dosing requirements and project optimists from the FDA that others will. Here's our study schema in head and neck cancer. We first did dose escalation. We locked on a couple of doses then, and we're doing combination doses at dose level five and six, as you can see here. Now we're doing this with Toripalimab. This is the study. This is 40 patients. We expect this study to read out in mid-year. Now, these results, I'll just discuss with you in just a moment, were revealed at AACR in 2025. There is a manageable safety profile with this product class, and this is very promising anti-tumor activity. Let me show you something very exciting here. On the left side of this panel, you see this green lit-up area in the upper left-hand quadrant. These are biomarkers. These are actual CCR8-positive Treg cells. You can see how they're there and the proliferation of those cells. Below, you can see the subsequent treatment after our moiety CHS-114, and you can see the diminution, and there's no green in the bottom left-hand quadrant. That means that the Treg cells were successfully depleted. What's important and what's really impressive here, though, is the next panel, the upper right. In the upper right, you see the CCR8. You see it's red. Okay? That's pretreatment. You can see now the infiltration of CD8-positive T cells into the tumor in the lower right-hand quadrant right here. This is really amazing. This is the first time that the actual supposition that depletion of Tregs in the tumor microenvironment would lead to subsequent infiltration by CD8-positive T cells. We are the first folks to show this. In this same study, we also saw a confirmed partial response of target lesions. Here you see a very large lung lesion. This is a fourth-line head and neck cancer patient. In this patient, this patient was refractory, had gotten a lot of therapy, right? This is a very large lung tumor from a head and neck patient. You can see the diminution of this patient's tumor over a three-month period in two different areas. This is really remarkable data and addresses the underlying supposition in theory that diminution of these Treg cells will lead to positive therapeutic responses. We are pursuing, and we have recently actually expanded our program with Tregs. This is an area, as I point out to you, where 70% of the cancers are candidates for this because of the—so we're doing this broadly here, and I'll just talk about these three cohorts for a moment for you with gastric cancer, esophageal cancer, and then colorectal cancer. In each of these cancers, we have arms that we are examining them, and we'll be turning over these data cards mid to late next year. The colorectal cancer is the most recent expansion. As I said, this is really a cancer that has gotten much worse. The prevalence, the incidence has gone up. It's reaching every younger patient, and it's a huge, huge issue. Esophageal and gastric are both good candidates. Gastric cancer, in particular, has already seen very strong data in the hands of others, in excess of a 60% overall response rate on a background of Toripalimab, actually, for a Chinese group. Esophageal cancer, we feel very positively about, particularly given the low PD-L1 activity of Toripalimab in esophageal cancer. This is very, very interesting. You'll see these coming out as we go forward next year, but we're very excited, and we feel very positive about the outcome for all of these. Now let me talk a little bit about casdozokitug, which is a first-in-class anti-IL-27. IL-27 plays a fundamental role in immune system mediation with respect to barrier tissues. Barrier tissues are comprised of liver, lung, kidney, things that are filtration systems for the body where you have pathogen invasion. This was brought forward by Christopher Hunter at University of Pennsylvania. What's very interesting about this is it can be a very targeted therapy. You can look at these various cancers, and you can look at how much IL-27 there is. Here, with this program, we've seen very good activity in liver patients and lung patients. I won't talk about the lung patients. Don't have any—won't go through those slides today, but it has very strong activity, monotherapy activity in squamous cell lung patients that we saw during the first studies. Demonstrated monotherapy responses, very good safety profile. The fact that there's IL-27 in these tissues gives you a very good idea of which ones to go after. Let me talk just for a moment here about IL-27 and how it works. Now, IL-27, interestingly, does three things. First of all, it promotes and upregulates the expression of checkpoints, LAG-3, PD-1. All the checkpoints, as you see in the left panel, get upregulated. This, of course, inhibits the immune response. We know that one of the key ways cancer is being addressed with immunotherapy these days is really to block PD-1. Each of these have become an opportunity for intervention therapeutically. The second thing that it does, as you see in the middle panel, is it downregulates all the pro-inflammatory cytokines, turns down the whole immune response within the tumor, okay? That includes gamma interferon and all the rest of the cytokines. Most interestingly, most interesting what IL-27 does is it liberates and upregulates and activates natural killer cells. This is another mechanism. People get really focused a lot on T cells and PD-1s and checkpoints, and everybody sort of went after that in the past few years. Natural killer cells are a key mechanism the body uses to take on tumors. This is one of the key things that it does. Now, we have a study going. First of all, we opened this study up. We did a—I'm going to talk to you about the data here in just a moment of casdozokitug on a background of Avastin, okay? So that's Avastin plus an anti-PD-1 and how that's going. We are currently prosecuting a study across two doses on a background of toripalimab, LOQTORZI, and bevacizumab. We've dosed these patients. The enrollment for this study is going very well, and we expect to get some answers on this around next year. Let me show you some of the data here. On the left side of this, you see the waterfall plot. What's really, really striking is the response rate. 60% of the patients had tumor shrinkage on initial scans. There was a 38% overall response rate, and significantly, there was a 17% complete response rate. On the right side, you see the spider charts. This is really incredible. Look at the duration of the response. These patients are actually still on therapy. How does this compare with standard of care? Here it is, the 17% complete response rate. That is about twice standard of care, which was Avastin alone, you see there for 7.7%. Also, you look at the ORR, 37.9% compared to the other ones. This looks like it is working very, very well in this patient population. We are very excited about getting this data a little later this year. We are seeking to replicate this data, improve on this, and then we are going to expand into other areas, including lung. Let me just spend a few moments then on one more topic, and that is the last topic, drugs, data, and deals. Let me just talk to you a little bit about our global rights. We were very successful in divesting our biosimilar franchise over the last year and a half. The company paid off $480 million in debt. We brought in almost $800 million with a divestiture of the biosimilars. We put $250 million on the bottom line. The result of that, we were able to move forward with all these. We also acquired Surface Oncology, who brought these assets forward I just talked about. This is a very interesting company. Surface Oncology was spooled up on the East Coast by some very, very scientifically rigorous folks. Over $300 million went into Surface Oncology since its founding. This company reached a peak market capitalization of over $950 million. We acquired this company for about $65 million in stock, closed that transaction two years ago, divested all our biosimilars, and repositioned our company. It is first-class innovative oncology. Regarding our opportunities here going forward, we are very keen on exploiting partnerships. In order to really provide a step change in patient survival for cancer, it requires combinations. Combinations require collaborations or partners. You cannot do this just with your own pipeline. One of the fundamental strategies that we have had is to take our PD-1 and put it in the hands of others to use it with their complementary assets. Same thing with our other products, for example, CHS-114. We will happily put that in the hands of other people. When they develop their bispecifics or they develop their T-cell engagers, they will do so, in our view, alongside our product. I think this is a very unique strategy, right? We do supply agreements, and we're also able to do ex-U.S. licensing over the next six, 12, and 18 months as we go forward. We look forward for that data to drive those deals. That'll do three things for us. First of all, it'll validate the pipeline and validate these assets and what I've told you here today. It'll provide us upfronts to offset our clinical spend. Also, in the longer view, what it'll do is allow us to offset the spending for the pivotal trials by spreading those costs globally. CHS-114 and these other novel combinations I talked about just a moment ago, we think these are very, very exciting. We're talking to a number of folks about this. These clinical collaborations with novel and approved moieties, we can either bring it in, use it with our studies, or we can provide it for their studies. This is a very cost-effective expansion strategy. Let me just summarize for you here the Coherus value proposition. I've talked to you about LOQTORZI, our drug, next-generation PD-1 commercial, doing well, fundamental active scaffold for us in our products. CHS-114, the tip of the spear on what is a very, very exciting and evolving new methodology for treating cancer, casdozokitug, first in class. We are pursuing a number of cancers: head and neck, gastric, colorectal, and so forth, and a number of licensing deals. Thank you for your attention today. If we have any questions, I'll just take a moment if you have a question. If not, my team and I are here and happy to chat. Thank you.