This morning, one of Baird's senior biotech analysts. Welcome to the Baird Healthcare Conference. Really excited to get things kicked off today with Coherus Oncology. The management team here is to my left are going to do a presentation, and looking forward to hearing the exciting story ahead. Thanks. Thank you, Brian. Thank you. I'm Denny Lanfear, Coherus's Chairman and Chief Executive Officer. To my left is Dr. Rosh Dias, the company's Chief Medical Officer. Let me first apprise you of the forward-looking statements and direct you to the company's regulatory filings for further details with respect to the products tagmokitug, casdozokitug, and LOQTORZI. Today, I'm first going to summarize for you the vision and the summary of the company, where the company is positioned in the cancer treatment paradigms. We'll spend a moment talking a little bit about overcoming immune resistance through T reg depletion. Of course, you're aware that we have a product, tagmokitug, which is in a number of phase I, IIs, about 6 indications by Dr. Dias and company. We'll spend some time with you today talking about that, the progress of those clinical trials, the mechanism of action, and what we have seen so far with that. We'll also talk to you a little bit about casdozokitug, which is our first-in-class IL-27 antagonist, which is in first-line liver cancer. Coherus Oncology is focused primarily in the arena of overcoming immune resistance. The post-administration of most chemotherapy agents, a cell type called T regulatory cells develops that I'll spend a little time on talking about today. In that context, this enforces immune resistance and keeps the immune system from attacking cancerous cells. This is going to be a key MOA going forward in oncology. Today, let me just summarize three key things for you. We are a commercial-stage innovative oncology company. We have a launched product, LOQTORZI, in nasopharyngeal cancer, where we are the only approved and available marketed product. I'll apprise you just in a moment about how we're moving forward with that in terms of our revenues and so on. As you see on the left side of this slide, we are advancing tagmokitug. This is a CCR8-positive Treg depletion mechanism. This product has very high selectivity. There's probably a half dozen of these products in the field right now moving forward. As I'll talk in a moment, Bristol Myers Squibb, Amgen, and some others have them. However, we believe that we have the best-in-class molecule for a number of reasons, including selectivity. We have a broad development program that we'll talk about in just a moment, as indicated across six different indications. More importantly, we are looking forward to data readouts this half of the year. In our last call in August, we discussed the progress with our head and neck study. Dr. Dias will give you some additional details on that today. We also have studies in gastrointestinal cancers, which include, of course, colorectal cancers. Importantly, we are also advancing this product in conjunction with Johnson & Johnson in metastatic prostate cancer. Casdozokitug is our IL-27 antagonist. This is a first-in-class product. This is a highly targeted program in first-line HCC. We have seen in the previous study very encouraging activity, including significant duration benefit with this product. We are now doing a randomized three-arm study at two doses; we will discuss it with you just in a moment, and we also have data readouts coming this half of the year. Lastly, as I indicated, LOQTORZI, our next-gen PD-1 inhibitor, a very unique mechanism of action here, binds on a very unique epitope of the PD-1 receptor, and has shown significant efficacy in nasopharyngeal cancer. Here is LOQTORZI. LOQTORZI has demonstrated significant clinical differentiation and survival. Here on the left panel, you see data demonstrating its activity in low PD-L1 esophageal cancer, for example, in contrast to Keytruda. As a matter of fact, this product is approved irrespective of PD-1 status, I should say, in Europe. In the middle panel, you see, for example, our very stellar six-year survival data. These patients live almost twice as long with LOQTORZI plus chemotherapy versus chemotherapy alone. This profound efficacy has been rewarded with top positioning on the NCCN guidelines. It is Category 1A, both in first-line in conjunction with chemotherapy and also in second-line as monotherapy. We have been focusing on the commercial execution of LOQTORZI in the nasopharyngeal space. This is about a $250 million opportunity all in considered. We project reaching a maximum of about $175 million annualized per year with this asset in 2026, and we expect to reach $15 million per quarter. This is important in terms of sales because at around $15 million per quarter, this product pays for the commercial opportunity, the COGS, the manufacturing, the royalties to our partner, and so on. Therefore, revenues beyond $15 million a quarter, say up to $30 million a quarter here in 2027, it starts to contribute to the company's SGA. Around $30 million to $35 million a quarter, which we project we will reach sometime in 2027, probably towards the end of the year, this will be sufficient to drive and cover the Core burn of the company, X, the clinical costs. Our objective here then is to finance the company with the core burn on LOQTORZI. We are very tightly focused on execution around this product. Lastly, ultimately, we think this product will reach, as I indicated, maybe $175 million a year or so. That is probably the $40 million-plus per quarter, at which time there is some additional funding for various things. Primarily, that is the role of this asset in the company together with the pipeline. With respect to the revenues and so on, the key issues that we are driving on this year is overcoming Keytruda, which has been entrenched in the market prior to our launch. Keytruda has broad utilization in head and neck. Nasopharyngeal cancer is treated by head and neck physicians. Our focus really is on educating physicians with the six-year survival data, having claims data, which will indicate to us which particular physicians and practices have patients, and then have a broader field footprint across thought leader liaisons, et cetera, and to be able to get to these physicians and educate them accordingly when the patients come up. Here is our pipeline, and I would just point out that the role of LOQTORZI in the pipeline is both as a revenue generator in the context of nasopharyngeal, but also revenue multiplier. Whenever any of these indications with either tagmokitug or casdozokitug are approved, we will register a sale both for that novel asset and LOQTORZI. Let me talk a little bit about overcoming immune resistance through T reg depletion. Tregs are immune-suppressive T cells that support immune homeostasis. They are broadly circulating in the body, but they are particular players in the tumor microenvironment where they inhibit the immune response. That is through the mechanisms of immune suppression, cytokine release, and lastly, the degradation of the activity of all of the immune system effector cells, natural killer cells, and so on. They are prognostic for lower survival and outcomes in the tumor microenvironment. There is therefore been the hypothesis that if T regs could be depleted in the tumor microenvironment selectively, then perhaps T cells and the overall immune system would recover and you would see beneficial response. That is exactly what we are testing across a number of indications. It is important to note that cytotoxic therapies, a number of them, chemotherapy, VEGFs, KRASs, radiation, ADCs, all result in the substantial generation of T regulatory cells. This is the body's natural response to destroying cancerous cells. This then is the secondary mechanism which kicks in, limiting immune response and thereby truncating duration. This is really important. Whenever you treat, you get a very substantial ORR with many of these therapies. However, they directly increase intramural T regs, upregulate T reg recruiting checkpoints, and induce suppressive signaling. What this results in then is a large unmet need to restore overall survival or extend overall survival. Particularly in terms of restoring potentially exhausted T cells and enhancing the immune profile. Again, this is what we are testing with our clinical trials thus far. As it turns out, in 2016, it was discovered that T regulatory cells in the tumor microenvironment have on their surface a protein called CCR8. It was therefore posited that if you could selectively attach to that CCR8 and you could enhance a depletion of a T reg cell with effector cells pursuant to that, then you would get rid of the T regs, particularly differentially in the tumor microenvironment, without having substantial impact on their role in the periphery enforcing normal immune homeostasis. On the left panel here, what you see is the distribution of T regs in the periphery versus the tumor microenvironment. On the right panel, you see the mechanism of action that these molecules now enhance. You have an antibody; it grabs the CCR8 on the surface of the T reg, and then this facilitates the effector cells destroying. As a matter of fact, before we get to that data, we will talk about one other thing. We've actually developed what's called TIRI, the Tumor Immune Regulatory Index, which is associated with these cells. It's important if you pursue this that you have a way of enriching the response and understanding that you're going after cancers in which CCR8 plays a key role in the tumor microenvironment, and we have done that. TIRI is a CCR8-derived index. It is very much akin to what you see, for example, with the PD-1s, with the CPS score. You have to have a certain CPS score in order to expect efficacy. That is because it is a targeted therapy. We're actually leading in this field, but as we roll out our data from now until the end of the year with our T reg depletion MOAs, we will refer to this as a way of understanding the response. Let me let Dr. Dias then talk to you a little bit about TAGMO, how it is differentiated from the other assets that are out there being developed by various companies, and so on. Rosh? Thank you, Denny. Tagmokitug is our CCR8 targeting antibody, and we believe, as Denny mentioned earlier, that this is potentially best in class because of many of the features that are outlined on this slide. We do have very high selectivity. We've screened over 5,500 cell surface proteins in order to get this molecule, and we've shown no off-target binding. Secondly, we've also shown some very good ideal pharmacological properties, and that includes high affinity, the picomolar range. It includes potency with enhanced ADCC and ADCP activity. We have a very broad development program, which I will outline in the next few slides, including being the first in combination with a T-cell engager, as well as the first CCR8 in prostate cancer. Then we've also shown proof of mechanism, which I'll show you in the next slide also. Denny mentioned that there are several CCR8s in play right now. There are also several that have been parked, in many cases because they haven't demonstrated some of these properties that we've been talking about. This is the tumor remodeling that I alluded to in the earlier slide, and this is from our phase I study, which focused in essentially on second-line plus head and neck squamous cell carcinoma. We presented this data at AACR last year, so in 2025. What you see on the left panel is monotherapy data, which shows this very nice tumor remodeling. On the top, pre-treatment; on treatment below. You see in green, the CCR8-positive Tregs within the tumor microenvironment really disappear on treatment. The second thing we saw was that the CD8s, so the cytotoxic T cells, infiltrate as well. You see this very nice infiltration of red, the CD8s coming in as well. When we added in toripalimab, and you see this panel on the right, when we added in toripalimab, with activation of those T cells, then we saw a very deep partial response in a fourth-line head and neck squamous cell patient. This is a patient who previously failed a PD-1, previously failed a taxane, as well as a TKI, and then responded to this combination. What you see here is a lung metastases from this head and neck patient, and you see this very nice diminution in tumor size over a four-month period or thereabouts. On the back of that, then, we expanded our program to what you see here, and we have two ongoing protocols and a third about to start. From top to bottom on the left panel, protocol 1 is further expansion of the second-line head and neck squamous cell program, focusing in on second-line specifically. I will say a few more words about that in the next few slides. Our second protocol is a GI protocol, which focuses in on four cohorts, so second-line upper GI adenocarcinoma, second-line esophageal squamous cell, first-line esophageal squamous cell, and a fourth-line plus CRC colorectal population. The protocol that is about to start is a novel combination protocol, which will have its first cohort as that prostate cancer protocol, again, Denny was alluding to, third-line plus population in combination with pasritamig. It is important to bear in mind exactly what we are looking for with each of these cohorts. For the second-line cohorts, that is head and neck, upper GI adeno, second-line esophageal squamous cell, we are looking to ask the question specifically, can we reverse immune exhaustion and rescue T cells? Because by and large, most if not all of these patients will have had a prior PD-1. With the first-line esophageal squamous cell cohort, we are looking specifically at the combination with chemotherapy. This is asking the question, can we combine safely and in an efficacious manner with chemo in order to be able to potentially move up earlier in the treatment paradigm? In the fourth-line plus CRC cohort, we are looking at essentially, can we turn a cold tumor hot? This is an area of high unmet medical need where the current standard of care gives you a very poor outcome. Then, of course, in the third-line plus prostate cancer cohort, we are asking whether we can safely and synergistically combine with a T-cell engager. On the basis of this, then, we will move forwards and determine how to proceed with the rest of our development program. We will select the appropriate tumor type to further development. We will use this program also then to inform on which line of therapy and immune context will give us the best path in terms of moving forwards, patient selection strategy, of course, and then combining with combinations as well. Let me just say a few more words about the head and neck cohort specifically, which we did talk about at our earnings call a couple of months ago. This is a further expansion, as I say, of head and neck squamous cell. This is focused in on the second-line specific population. We're looking at 40 subjects, two doses of tagmokitug in combination with toripalimab. We had completed accrual earlier this year. We anticipate giving you further information in terms of a full data readout in October, so next month. What we have communicated so far is that we have seen good safety and an acceptable and manageable safety profile, first of all. Secondly, we also communicated that we have seen activity both in terms of response but also in terms of durability as well. Thirdly, that we have seen enrichment of activity, that is greater activity in the HPV-positive subpopulation, as well as those patients who have a high Tumor Immune Regulatory Index score that Denny talked about earlier. Bear in mind, of course, that HPV positive is where the relative white space in the developmental environment really is. Many of the EGFR bispecifics, for example, are either focused in or their benefit is driven by HPV-negative patients. More to follow in October. This is the remainder of our program in a little bit more detail from the previous slide that I showed you. We've talked about the second-line head and neck cohort. Moving from left to right, our second cohort, or our second protocol, I should say, is in GI cancers. Cohort A of that is the upper GI adeno population, which is second-line gastric GEJ esophageal adenocarcinoma population. Again, 40 subjects, two doses of tagmokitug in combination with toripalimab. This, I'll remind you, is where the field has shown some efficacy, probably bookended by, on the upper end, LaNova Medicines, a Chinese company with data from China showing roughly a 36% ORR, and bookended on the bottom end by Amgen, which has demonstrated an 8% ORR there as well. We're excited about this cohort and looking forward to seeing the data mature more. The second-line population in esophageal squamous cell is specifically looking at 20 subjects. Again, two doses of tagmokitug in combination with toripalimab. The first line, as I mentioned, is a safety cohort looking at the combination with chemotherapy. The colorectal cancer cohort is looking specifically at a fourth-line plus MSS population, asking the question again, can we turn this cold tumor hot? We are looking initially the non-liver mets population. We have recruited our initial 20 subjects and completed accrual. Our prostate cancer program then we are looking to kick off in the next couple of months or so. Thank you, Rosh. Just before we leave the tagmokitug-Keytruda, perhaps you could just comment briefly on the side effects and the tolerability profile that we have seen with tagmokitug with toripalimab vis-a-vis the other CCR8 agents that are in the field and what has been presented. Yeah, absolutely. So what we've presented at AACR in our early-stage program is, as I said, a manageable and acceptable safety profile. What we've seen is in terms of the grade III plus events has essentially been some lipase elevations, but no overt pancreatitis, which is really what you look out for. We've also seen some elevations in terms of LFTs, again isolated and reversible as well. So, we're encouraged by what we've seen so far, and we continue to watch the program as it evolves because, of course, the ongoing program right now is a larger number of patients. Good. Lastly, any additional color on the prostate study with J&J's agent pasritamig in terms of timing and what we expect to see, and what that would indicate for future development with T-cell engagers? Yeah. So we've designed this third protocol now as a novel combination protocol. So it's got multiple cohorts, but the first cohort will be and is this combination with pasritamig. Pasritamig is J&J's T-cell engager. It has shown in some encouraging early data in metastatic castroresistant prostate cancer, late lines in particular. They showed some data at ASCO last year to that effect. So this is a combination we're excited about. We anticipate starting it in the fall timeframe, which is what we've communicated. We're on track for that start. We should see some data probably in the first half of next year. Based on that, we'll figure out how best to proceed in terms of both safety and efficacy. Thank you. Let's talk a little bit about casdozokitug, which is a very interesting molecule. This target, IL-27, was actually brought forward by Chris Hunter at University of Pennsylvania. Very interesting. This asset is first in class and actually only in class. What Dr. Hunter discovered is an underlying role with IL-27 in the context of immune response and invasion. IL-27 has a key role in terms of turning off immune response, secondary to pathogen invasion. It does this really in three ways. It first upregulates these various checkpoints, LAG-3, PD-1, and so forth, and thereby turning off T-cells. The other thing that it does is also moderates the activity of natural killer cells, which are key effector cells in the environment. The other thing, lastly, what it does, it downregulates pro-inflammatory cytokines, interferon gamma, et cetera. Very interesting and tellingly, in animal models where IL-27 is knocked out, what occurs is that the immune response happens subsequent to pathogen invasion, and the body responds, but it does not turn off, and the animals subsequently die then of autoimmune disease. This is actually very interesting. The objective of this study and this exploration really is to understand that if you antagonize IL-27, what will be the effect on any cancers, particularly in these barrier tissues such as liver, lung, and kidney. I'll let Dr. Dias talk about this study. This is the data that we have already communicated from our complete study. We showed this data at ASCO GI last year, 2025, again. What we did was we added on in our initial program, casdozokitug, to the current standard of care, atezolizumab and bevacizumab. These are the top-line data that we showed. What we showed was a 38% overall response rate. For context, atezolizumab/bevacizumab alone in IMbrave150 has given a 30% ORR. We also showed a complete response rate of 17%. Again, for context, atezolizumab/bevacizumab in IMbrave150, 7.7%. Of course, these are cross-trial comparisons, so bear that in mind, but nevertheless, pretty encouraging in terms of what we saw. PFS was 8.1 months. The activity that we saw was irrespective of etiology, so we saw activity both in viral as well as non-viral disease, which is important for geographic applicability. The safety profile was very consistent with atezolizumab and bevacizumab alone. What we see on the right side of the chart here then is the durability. The spider plot shows that these results were pretty durable. The initial drop we think is due to the VEGF effect, and then the durability we think is added on by the casdozokitug. So we look forward to seeing the data with the ongoing trial, which I show you here. This is the ongoing trial, and what we've done here is essentially we've swapped out atezolizumab for toripalimab. So we are progressing a three-arm study now, two doses of casdozokitug in combination with toripalimab plus bevacizumab, which is intended to provide data to help with Project Optimus, and then Arm C is toripalimab plus bevacizumab alone, again intended to provide data to help us with contribution of components. So three arms, 72 subjects. We are looking at biomarkers as well, including ctDNA, IL-27 levels as well, because of course, IL-27 level expression is very prevalent in these barrier tissues like lung and liver. In terms of the current standard of care, that is atezo/bev. I have talked about some of the benchmarks there that we are looking at. But again, we anticipate that the benefit here will be mainly in terms of durability. So we are really waiting for this data to mature. The trial has completed accrual. It is a multinational trial based in Asia-Pac as well as in the U.S., and excited about the data to mature further, and we anticipate data towards the end of this year as the data does mature. I will end here by passing it back to Denny. Yeah, thanks, Rosh. Let me just summarize briefly where we are with our development programs as Dr. Dias briefed you. Tagmokitug, we have six indications going forward. Most of those we will get to this year, some next year. We are getting the initial data now. We have started to talk about the head and neck study. I think it is very interesting with the data with the CCR8 positives, and particularly in head and neck, which is HPV positive. We look forward to the other readouts. We also look forward to casdozokitug, which I think has a particular potential. What I really like about this particular asset, though, while tagmokitug is potentially very broad across indications, this is very highly focused with a very sharp mechanism of action, very strong initial data, and the opportunity for enrichment with IL-27. Lastly, LOQTORZI with our dual-pronged strategy there. Number one, to drive the business up over the next year or two to cover the cost of the company, and then secondarily, as a combination agent for the other assets in the pipeline. Thank you very much.