All right, we'll go ahead and get sta rted. Good afternoon, everyone, and welcome to the inaugural Citizens Life Sciences Conference. Inaugural because it's our first time in Miami, not the first time we're having a conference. But it's my pleasure to welcome Denny Lanfear from Coherus Oncology. Coherus is quite a unique company, right? They already have a product that's on the market and selling. They're an IO company. They have a deep pipeline of IO products. Here to tell us more is Denny. I'll let you have it. Thank you. Thank you, Ren. Thank you very much. Thank you all for joining me today. I have a few slides, so I'll go somewhat quickly through the slides and hopefully provide you with additional time to ask questions, talk to my colleagues. Let me first apprise you of the forward-looking statements and direct you to the company's SEC filings. I'll talk today about how we now have positioned the company as an innovative oncology company focused on overcoming immune resistance in cancer. I'll talk about the product strategy, which I think is very unique, as Ronnie alluded to, and then go on a little more specifics about the products and what we expect to get done here in 2026. Coherus in its transformation acquired Surface Oncology in 2023 in Septe mber. We straightforwardly moved into divesting of our biosimilar assets. With Surface Oncology came two very interesting products. One, tagmokitug, a CCR8 Treg depleting molecule, which has significant potential therapeutic utility across a number of indications, and casdozokitug, which is an anti-IL-27, which has manifested very strong efficacy in barrier tissue cancers, such as liver. We divested our biosimilar assets. We paid down nearly $480 million in debt. We put $250 million in the balance sheet and then began the very aggressive development of these products. Let me just make one more key point here from the financial side of the business. The divestiture of UDENYCA to Intas resulted in both an upfront payment of $483 million, but also, importantly, $75 million in follow-on payments that are due end of this year and early 2027, which we have a significant degree of confidence in earning. This is our story focused on the products, of course, the clinical trials that we have underway, which will read out this year, and then the deals that we are moving forward with. Most recently, we concluded a collaboration agreement with J&J with tagmokitug, and I'll talk to you in just a moment about that for a T cell engager in prostate cancer. That's the first CCR8 to go into prostate cancer and the first to be combined with a T cell engager. LOQTORZI is an interesting story, and I'll talk about that next. Let me just devote just a moment to the data development. My chief medical officer, Dr. Rosh Dias, is very busy with a number of studies, head and neck cancer with tagmokitug in conjunction, or I should say in combination with, toripalimab. As it turns out, T-regulatory cells are problematic across the gastrointestinal tract. We are looking at esophageal cancer, gastric cancer, colon cancer, et cetera. As I indicated, now prostate cancer in conjunction with J&J. Casdozokitug, as you can see, is in HCC, hepatocellular carcinoma, and we expect that to read out mid-year also. I'll summarize for you some very promising results from the early studies. This is our pipeline. I'll just double-click on this for a second. There's one key takeaway with this. First of all is the role of LOQTORZI in our pipeline as both a revenue generator in the context of nasopharyngeal cancer, which I'll talk about in just a moment, but also a revenue multiplier. As you'll note, our pipeline is being developed in combination with toripalimab. What that means is at point of sale later when these are approved, we have expanded indications for LOQTORZI as we get our pipeline approved and therefore get substantial increases in sales, which you see here. Because of this, the company is targeting some $33 billion with just the trials underway in the U.S., where we operate at this time. Let me spend a moment on LOQTORZI, our backbone PD-1 product. LOQTORZI is very interesting. It's a next-gen product for a couple of reasons. First, very high affinity binding to PD-1. Secondarily, that affinity is focused at something called the FG loop, which is a particularly interesting part of the PD-1 epitope and results in a significant amount of internalization of PD-1 off the surface of the T cell. This product has shown in vitro studies to be much more active than the standards of care, KEYTRUDA, and OPDIVO. It is because of this very unique signaling in the T cell that does this. Because of this, it's also been active in low PD-L1 cancers. You can see here the esophageal data where the hazard ratios are very much the same. I would just point out that LOQTORZI is actually labeled in the EU for low PD-L1 esophageal, whereas in the US, both KEYTRUDA and OPDIVO lost their labels in low PD-L1 esophageal cancer. In a moment, I'll talk to you about a study Dr. Dias is pursuing in esophageal cancer in combination with Toripalimab with tagmokitug. So this efficacy has translated very importantly to patient benefit. Just on the left side of this, I'll just make a point about the six-year survival data, which you'll see here is 64.8 months. This data was just recently disclosed at the end of last year, versus 33.7 months for patients on chemotherapy alone. A truly significant benefit if you're a nasopharyngeal cancer patient with metastatic nasopharyngeal cancer. This sort of data and efficacy has earned us top ranking on nasopharyngeal NCCN guidelines, as you can see in the right part of this panel. Importantly, though, this has translated to patient benefit and our ability to communicate this patient benefit to physicians and resulting increases in sales. We're very proud to say that in the period of 2025 over 2024, we were able to more than double sales of LOQTORZI from some $19.1 million to $40.8 million over that period and step it up very systematically each quarter. Our target is to ramp this up about 10%-15% per quarter. We did a little better than that in 2025, and that is our focus going forward. I'll double-click on a couple other things on this slide because I think it's quite important to keep in mind. The first is that we project, and I think quite reasonably, that we will achieve our peak market share sometime in 2028, and this is about a $250 million market. We project reaching about 70% market share in 2028, some quarter within then. That's about $43.75 million per quarter, and that's an annualized $175 million. Along the way, a couple of key things. First, LOQTORZI will contribute significantly to the overall SG&A of the company. It'll... Once it gets to where it's doing $30 million-$35 million per quarter, the core burn of the company, that is all the people, the commercial costs, and so on, will all be paid for. That does not include, however, things like clinical costs and development costs and other such thing which we put in a separate bucket. Also, we project that this will occur sometime in 2027. We project that we'll get to the point where this will be a positive contributor to have taken care of that. I'd also note that we are also guiding that during 2026, we'll reach about $15 million-$16 million a quarter with LOQTORZI, at which point the overall commercial costs will be paid for. This includes things, for example, like COGS, a royalty to our partner, Junshi, another small royalty, the commercial team, all the commercial team's costs, their computer systems, et cetera. Those are the next two stop posts along the way to reaching maximal market penetration. Now, we made some significant investments to our commercial team over the past quarter. As you probably know, we raised $50 million and just closed on that a few weeks ago. That is one of the key things that we did in the context of use of funds for that is contribute about $10-$15 million for the commercial team. We added an additional AE or salesperson per region. There are four regions. We now have six per region. We added an inside sales force, one person per region, a dedicated person for Veterans Affairs, which is hard to penetrate, and some other points. We wanted to make sure that we were fully deployed against the objective of getting to maximal market share as fast as possible, so we made these investments. We also made investments in the computer systems and information systems to facilitate this. This is, of course, a rare disease, which means you first have to find the patients because you want to find the diagnostic codes. You have to buy all that data. You have to project that data up through the dashboards and viewing systems for the sales team to view and then go pursue the healthcare providers. We've also increased our investments here, both in terms of data acquisition and going from, for example, 30%-35% of these alerts in 2025, up to 65%-70% of these alerts going forward now during the two-year planning period. We think these are prudent investments to make because we really wanna pull forward the maximal market penetration time. Let me talk a little bit about tagmokitug, just briefly. While the progress with immune therapies has been very exciting over the past 10 or 15 years, there's still about 70% of these patients that are not treatable and for reasons such that there's no T cells or they're PD-L1 negative, et cetera. There's very high unmet need. T-regulatory cells are particularly problematic and are associated with very poor prognosis across tumors. Here on the left panel, what you see is a graph showing you two things. There's a number of cancers, and you see here the ones that are in red are the ones that we have currently under investigation. There's a number of these cancers. It shows two things. Number one, the density of CCR8 positive Tregs, and then secondarily, what% of those Tregs are CCR8 positive. Both of these are important considerations that we're trying to elucidate with respect to our clinical program. Excuse me. Now, Tregs play a fundamental balancing role in the immune system. You know, the immune system has to respond to insults, but then it has to be turned off. So your body is in a constant state of immunological homeostasis, and Tregs do that. Our company is focused on overcoming immune resistance in cancer because cancer uses the inherent immune system to isolate itself from immune response, and that is where we look. So, we've made great progress with these Tregs. I would just say that this is such an interesting and topical area of investigation that it was the subject of the Nobel Prize last year. If you were to use Tregs therapeutically and clinically, there's three key criteria that you have to keep in mind for efficacy. You know, first of all, you have to achieve significant Treg depletion in the tumor microenvironment with a Treg depleting agent, and you see here that we have demonstrated that in tissues. I'll show you some very interesting graphical data in just a moment. Then you need the subsequent infiltration of CD8+ T cells to attack the tumor. This is the so-called remodeling where the Tregs go down and then the CD8+ T cells commence that can attack the tumor. We've shown that. Importantly, the T cells have to be active and they have to be. There's a number of ways they can be activated, whether, you know, binding to T cell engagers or PD-1s, but they must be active, and they can't just be exhausted. This is very important, and this is why we're elucidating the interplay between these various factors with our clinical trials. Tagmokitug is highly selective, potentially best in class. It is only, it's the only known CCR8 that shows no off-target binding. It has excellent pharmacokinetics, high affinity. This is probably the most important slide in my entire presentation. This was data that was presented at AACR last year. On the left panel here, what you see is tumor biopsy tissue. This is head and neck cancer, and these are head and neck cancer patients that we were doing a study with Tagmokitug. What you see in the green there, pretreatment in the upper left is CCR8. You see it's bright green. Then you see subsequently post-treatment, the depletion and all the green is gone, meaning that the Tregs, the CCR8 positive Tregs are gone. At the same time, importantly, you see the CCR8 the CD8+ T cells, and you can see the infiltration of the T cells, the high proliferation and infiltration in the lower right panel. This is very, very important. This tumor microenvironment remodeling is extraordinarily and is something that people hoped was achievable. In the same study, in an adjacent arm, patients were treated additionally with our PD-1, toripalimab. You see here a tumor 2.8 cm which is a golf ball-sized tumor, in a patient's lung, a metastasis in the lung from a head and neck cancer patient. You can see the diminution of this tumor over three to four months in these scans. This was just incredible validation of the role of Tregs and the importance of remodeling in these patients. This then gave us confidence to pursue additional studies with tagmokitug. Indeed, it gave J&J confidence to engage with us and work with us in prostate cancer. This is our clinical program with tagmokitug, our anti-CCR8. As I indicated earlier, you can see it's in three parts. You know, the first is the gastrointestinal cancers. Here you see in gastric second line, you know, GC and so forth. And then you see the head and neck cancer studies and finally prostate. What's important to note is we think there's significant clinical justification for all these studies, particularly in gastric cancer. Another team, Hengrui, in China did a study with a CCR8 in second-line cancer patients and saw a 36% overall response rate, which is very interesting. Also on a background of toripalimab, remarkably. We're also pursuing esophageal in two different, first line and second line, as well as colorectal. I just indicate that the colorectal study we got to sometime near the end of last year. We decided to activate that after we saw the head and neck cancer biopsy data, and that's moving along, but we won't have data for that till the end of this year or maybe even early next year. The other two, as you see, we're projecting we'll have data by mid 2026 or second half of 2026. The head and neck cancer study is moving right along. Again, all these are about $4 billion opportunities. Dr. Dias and his team are having very strong enrollment here. Again, the tagmokitug plus toripalimab and then the prostate, third line, prostate cancer, in conjunction with J&J. That study, we just agreed to, so we probably won't get that spooled up until the second half of this year, and we expect to see data in the first half of 2027. Extremely excited about that. You know, if I go up to 50,000 ft for a minute and just talk about what are the more broader therapeutic applications of T regulatory cell depletion in cancer, it's important to note that T regulatory cell proliferation occurs after and subsequent to other cancer therapies. I would direct you to my colleague, Dr. Theresa LaVallee, my Chief Scientific & Development Officer, and her presentation yesterday on our earnings call where she talked about this. Tregs are very broadly across cancer, a problem. They're a problem with ADCs, problem with T cell engagers, problem with radiation, all of these. There's a lot of Tregs. We feel that this is a very important area of investigation, and our ambition is to become the Treg depleter of choice, across therapeutic areas, and you can see why. Now let me just show you here how the T cell engagers work, because I spoke for a minute about the J&J agreement. You can see what T cell engagers do and on the one hand, one part of the molecule grabs the cancer, the other part grabs a T cell. If there's not a T cell to grab onto because there's too many Tregs in the tumor microenvironment, then you'll have limitations of efficacy, presumably. This is why J&J was so excited when they saw this data, the depletion of Tregs, you know. Indeed, Treg proliferation is a problem across cancer, and did this agreement with us. We talked to them, you know, after the presentation in April and May of AACR, then again in November, and I would just really want to thank J&J for pursuing this so enthusiastically with us. It only took us a couple of months to put this together, which is very rapid for a big company. This is the first time that a T regulatory depleter has been used with a T cell engager, and this is also the first time for prostate cancer. Let me turn a moment then to the other pipeline product we have, casdozokitug, which is, you know, probably my own personal favorite. CASDO is a first-in-class IL-27 antagonist. We are both first in class and only in class. IL-27 is very interesting and plays a key role in cancer and barrier tissues. Why? You know, now you have pathogen invasion in barrier tissues. That's the one thing that happened, for example, when you breathe or things get filtered through your liver. There's a lot of pathogens, of course, which occur. The immune system responds to these pathogens, but it has to be turned off. Again, homeostasis is the key. To overcome immune resistance means you have to rebalance this homeostasis. What IL-27 does is threefold. First of all, it results in the proliferation, this upregulation of these checkpoints, all the usual suspects, PD-1, LAG-3, TIGIT, et cetera. You know, this is a big off switch, correct? The downregulation of the pro-inflammatory cytokines, you know, interferons, et cetera. Lastly, and probably more importantly, you know, constraining the activity of natural killer cells, which doesn't get nearly as much attention as the checkpoints, but is very important. This is a threefold, very, very powerful system for turning off immune response. If you knock out an animal for IL-27 and you infect them, they do not die of infection. The infection is dealt with. They die of autoimmune disease because the immune system does not get turned off. Dr. Dias has been performing an investigation with our anti-IL-27 agent in first-line HCC, and you see the very impressive data here. 11 objective responses, 5 complete responses, a 17% complete response rate, 38% overall response rate. What you see in the spider chart on the right side of this is very impressive also. Not only do you have these responses, but they are durable. There's patients out for years on this. This compares very favorably to existing standard of care. I'll direct you to the left panel of this slide, where you see the 38% overall response rate as it compares to some of the other, standards of care. Take a look at the complete response rate, the 17%. This is very impressive, and we hope to duplicate this. Indeed, this is our follow-on study, which we have going right now. Again, I say that enrollment's moving along well, so we hopefully will get some data later in the year as we indicated. This has two doses of casdozokitug to comply with Project Optimus, both on a background of toripalimab, like Torzi, against just toripalimab and bevacizumab alone. The standard of care here is atezolizumab, bevacizumab being an anti-PD-L1, not an anti-PD-1. Toripalimab has shown very good efficacy equivalent to standard of care with bevacizumab previously in Chinese studies, so we're confident that exchanging toripalimab, or exchanging atezolizumab, I should say, for toripalimab will work out well. Let me talk just really briefly here about how we're going to summarize the year, then I'm happy to take your questions. You know, first of all, I think that we have assembled a very elegant strategy with a foundational PD-1 differentiated, next gen, that is commercially launched, that is producing revenues which are growing, which can significantly offset the burn of the company in the years to come. As a matter of fact, in 2028, it'll actually take care of that for us, the non-clinical burn. Two very promising agents, as you can see, one being brought forward very broadly across a number of cancers, with Tregs being an important mechanism of action, by the way, which we expect others to report on this year. Casdozokitug, showing very, very promising data in first-line HCC. The data readouts all coming this year. I think we've been quite busy in prosecuting the development of these trials. Last, I haven't talked too much about it, but we e xpect to do further collaboration agreements with others with tagmokitug with their agents, radiotherapy, ADCs. We have those conversations, you know, ongoing. We intend to pursue ex-U.S. licensing with both these products. It's important to note that we have global rights, which means we can once we get the data and we can get some transactions done, we expect to bring in modest upfronts and then have our ex-U.S. partners pay their share for their part of the pivotal clinical trials, making their costs very manageable for us. With that, I'll just stop for a moment, and I'm happy to take your additional questions. I think we have can probably throw one question your way, and I have my mic in case you want Teresa to answer. You know, I guess two quick ones. One, the data that's coming up, right? That we're expecting by the middle of this year. What kind of you know, how many patients worth of data? What kind of data do we wanna see that you need to see to make that kinda go, no-go decision to more advanced studies? Teresa, that is the question, and so I'll let Dr. Lavallee answer that. Thank you, Ren. Thanks, Ren. For the CASDO and KEYTAG, which is a randomized phase II, it's a follow-on study. Repeating the efficacy, that high CR rate that we saw in the earlier study, as well as the safety. People forget how important safety is in the front line for an overall survival endpoint in a registration study. Seeing those outputs would really set us up to have conversations for pivotal studies. That's the HCC data, and I just wanna remind folks that the data evolved over time. The initial read in mid-May just show equivalency between CASDO versus Tori Bev 'cause it took an additional six months for that depth of response and improvement in ORR. Seeing the first interim look as equivalent would be good and then wait for it to deepen by the end of the year. The other studies for TAGMO/KEYTAG are mostly designed with that 40-patient look, both to address Project Optimus as well as if we see benchmark efficacy with both ORR and duration of response. We get so focused on tumor shrinkage and forget that survival is what we're looking for, would set us up for favorable regulatory strategies. Importantly, you know, 'cause everyone's like, "Which tumor type do you like?" This is a very intentional program that's designed for us to learn the best context for this targeted therapy. Is it the density? Is it the percent of CCR8 T-regs? Is it the ratio? And what context will give us the highest efficacy read to then prioritize tumor types for other phase II studies? I think it's both what do we learn and are we set up to run, or are we set up to go into a different development plan that would expand on the data set we see? Excellent. Terrific, guys. Thank you very much for coming. Thank you. Thank you very much.