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Welcome to the Bayard Health Care Conference. Really excited to get things kicked off today with Coherus Oncology. The management team here 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 Lamphere, Coherous' chairman and chief executive officer. To my left is Dr. Raj 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, Tegmon Ketog, Kesdozo Ketug, and Lactorsi. So 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-regulation. Of course, you're aware that we have a product, Tagnol-Ketur, which is in a number of Phase I and IIs, about six indications by Dr. Dias and company. So 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 Casdoketrid, which is our first in-class IL-27 antagonist, which in first line liver cancer. Coherence 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 that I'll spend a little time on talking about today, and in that context, this enforces immune resistance and keeps the immune system from attacking cancer cells. And this is going to be a key MOA going forward in oncology. So today, let me just summarize three key things for you. We are a commercial stage innovative oncology company. We have a launched product, Lactorsi, in nasopharyngeal cancer, where we are the only approved and available market product I will prize you this 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 tagging with each other this is a CCRA positive T reg depletion mechanism this product has very high selectivity there's probably half dozen of these products in the in the field right now moving forward and as I'll talk in a moment, BMS, Amgen, 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. And more importantly, we are looking forward to data readouts this half of the year. In our last call in August, we discussed 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. And importantly, we are also advancing this product in conjunction with Johnson & Johnson and metastatic prostate cancer. Gastozo-Ketog is our IL-27 antagonist. This is a first-in-class product. This This is a highly targeted program in first-line HCC. We have seen in the previous study a very encouraging activity, including significant duration benefit with this product. We're now doing a randomized three-arm study of two doses. We'll discuss with you just in a moment. And we also have data readouts coming this half of the year. And then lastly, as I indicated, Lactorsi, our next-gen PB1 inhibitor, a very unique mechanism of action here, binds on a very unique epitope of the P1 receptor, and has shown significant efficacy in nasopharyngeal cancer. And here is Lactorsy. Lactoresy 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 Petrura. As a matter of fact, this product is approved irrespective of PD-1 status, PD-01 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 Lactorsi plus chemotherapy versus chemotherapy alone. And 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've been focusing on the commercial execution of electoresy in the nasal pharyngeal 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, we expect to reach $15 million per quarter. Now, this is important in terms of sales because at around $15 billion per quarter, this product pays for the commercial opportunity, the cogs, the manufacturing, the royalties to our partner, and so on. So, therefore, while revenue is beyond $15 million a quarter, say up to $30 million a quarter here in 2027, it starts to contribute to the company's SG&A. Around $30 to $35 million a quarterly, which we project we will reach sometime in 2026, probably towards the end of the year, this will be sufficient to drive and cover the core burn of the company, X, the clinical cost. So our objective here, then, is to finance the company with the core of Byrne on Lactorsi. And so we're very tightly focused on execution around this product. And then lastly, ultimately, we think this product will reach, as I indicated, maybe $175 million a year or so. That's probably $40-ish plus million per quarter, at which time there is some additional funding for various things. But primarily, that is the role of the company, the role of this asset in the company together with the pipeline. Now, with respect to the revenues and so on, the key issues that we are driving on this year is overcoming Cotruda, which has been entrenched in the market prior to our launch. Coturda has broad utilization in head and neck. The nasopharyngeal cancer is treated by head and neck physicians. So 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, 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 Lactorsi in the pipeline this both as a revenue generator in the context of nasopharyngeal but also revenue multiplier so whenever any of these indications with either tagnol ketog or castazoketog are approved we will we will register a sale both for that novel asset and lactorsi let me talk a little bit about overcoming immune resistance uh through t-reg depletion um t-reggs are immune suppressive of T cells that support immune homeostasis. They're broadly circulating in the body, but there 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. So there has therefore been the hypothesis that if Tregs 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. And that is exactly what we are testing across a number of indications. It's 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. So this is the body's natural response to destroying cancer cells. And this then is the secondary mechanism which kicks in, limiting immune response, response and thereby truncating duration. So this is really, really important. So whenever you treat, you get a very substantial ORR with many of these therapies. However, they directly increase intramural Tregs, upregulate Treg recruiting checkpoints and induce suppressive signaling. So 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. And 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. And it was therefore posited that if you could selectively attach to that CCRA and you could enhance a depletion of a Treg cell with effector cells pursuant to that, Then you would get rid of the Tregs, particularly differentially in the tumor microenvironment, without having substantial impact on their role in the periphery, enforcing normal immune homeostasis. And on the left panel here, what you see is the distribution of Treg's in the periphery versus the tumor macroenvironment. And on the right panel, you see the mechanism of action that these molecules now enhance. So you have an antibody, it grabs the CCRA on the surface of the Treg, and then this facilitates the effector cells destroying. And as a matter of fact, we've actually, before we get to that data, we'll talk about one other thing. We've actually developed what's called TIRI, the Tumor Immune Regulatory Index, which is associated with these cells. So 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. We have done that. So TIRI is a CCR 8 derived index. It is very much akin to what you see, for example, with the PD1s, you know, with a CPS score. You have to have a a certain CPS score in order to expect efficacy. And so that's because it is a target therapy. And we're actually leading in this field, but as we roll out our data from now until the end of the year with our Treg depletion MOAs, we will refer to this as a way of understanding the response. And let me let Dr. Dias then talk to you a little bit about TAGNO, how it is differentiated from the other assets that are out there being developed by various companies and so on. Rush. Thank you, Denny. So Tagma Ketog 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. So we do have very high selectivity. We've screened over five and a half thousand cell surface proteins in order to get this molecule, And we've shown no off-target binding. Second, 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. and 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. So this is the tumor remodeling that I alluded to in the earlier slide, and this is from our phase one study, which focused in essentially on second line plus head and neck squamous cell carcinoma. And we presented this data at AACR last year, so in 2025. And what you see on the left panel is monotherapy data, which shows this very nice tumor remodeling. So on the top, pretreatment, on treatment below. And 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. And you see this very nice infiltration of red, the CD8's, coming in as well, when we added in toripalamab, and that you see this panel on the right, when added in, toripalimab, with activation of those T- cells, then we saw a very deep partial response in a patient who has, in a fourth line, head and neck squamous cell patients. So 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. And what you see here is a lung metastasis from this head and neck patient, and you see this very nice diminution in tumor size over a four-month period or thereabouts. So 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. So from top to bottom on the left panel, protocol one is further expansion of the second line head and neck squamous cell program, focusing in on second line specifically. I'll 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 and then the protocol that is about to start is a novel novel combination protocol which will have its first cohort as that prostate cancer protocol that again denny was alluding to third line plus population in combination with pasoridomac it's important to bear in mind exactly what we're looking for with each of these cohorts. So for the second line cohorts, that is head and neck, upper GI adeno, second line esophageal squamous cell, we're 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 esrophageal esquamous cell cohort, we are looking specifically at 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're looking at essentially can we can we turn a cold tumor hot and this is an area of high unmet medical need where the current standard of care gives you a very very poor outcome and then of course in the third line plus prostate cancer cohort we're asking whether we can safely and synergistically combine with the t-cell engager on the basis of this then we'll move forwards and determine how to proceed with the rest of our development program we'll select the appropriate tumor types for the development we'll 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 so 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 so 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 tagma ketog in combination with tory palimab we had completed a cruel earlier this year we anticipate giving you further information in terms of full data readout in october so next month but what we have communicated so far is that we have seen good safety and an acceptable and manageable safety profile first of Secondly, we also communicated that we have seen activity, both in terms of response, but also in terms durability as well. And then thirdly, that we've seen enrichment of activity, that is, greater activity in the HPV-positive subpopulation, as well as those patients who have a high TIRI score that Denny talked about earlier. And bear in mind, of course, that HPV positive is where the relative white space in the developmental environment really is. of the EGFR bispecifics, for example, are either focused in or their benefit is driven by HPV negative patients. So 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. So we've talked about the second line head and neck cohort. Moving from left to right then, our second cohort is, 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 tagbo in combination with tori and this i'll remind you is where the the field has shown some efficacy probably bookended by on the upper end lenovo 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. So 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 TAGMA in combination with TORI. And the first line, as i mentioned is a safety cohort looking at the combination with chemotherapy and then 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 and we are looking initially the non-livermets population we have recruited our initial 20 subjects and completed accrual and our prostate cancer program then we are looking to kick off in the next couple of months or so thank you rash um just before we uh just before We leave the uh tagmo ketog uh perhaps you could just comment briefly on um the side effects and the tolerability profile that we have seen with techno key to vis-a-vis the other uh ccra uh agents that are in the field and and what has been presented yeah absolutely so what we've presented at acr in our early stage program is as i said a manageable and acceptable safety profile and what we're seeing is in terms of the grade three plus events has essentially been some lipase elevations but no overt pancreatitis which is really what you look out for and we've also seen some some elevations in terms lfts again isolated but and reversible as well. So, you know, 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. And then lastly, any additional color on the prostate study with J&J's agent Pazri in terms of timing and what we expect to see, and then what that would indicate for future development with T-cell engagers? Yeah, so we've designed this third protocol now then as a novel, novel combination protocol. So it's got multiple cohorts, but the first cohort will be and is this combination with Pasiridomig. Pasirido-Meg is J&J's T-cel engager. It has shown in some encouraging early data in metastatic, castor-resistant prostate cancer, late lines in particular, and 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 time frame, 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. And based on that, we'll figure out how best to proceed in terms of both safety and efficacy. Thank you. So let's talk a little bit about which is a very interesting molecule. So this target IL-27 was actually brought forward by Chris Hunter at Penn. Very interesting. This asset is first in class and actually only in class. And what Dr. Hunter discovered is the underlying role with IL- 27 in the context of immune response and invasion. And IL-27 has a key role in terms of turning off immune response, secondary to pathogen invasion. And it does this really in three ways. It first upregulates these various checkpoints, LAG3, BD1, 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. And the other thing, the lastly, what it does, it down regulates 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 of autoimmune disease. And so this is actually very interesting. And so 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. And I'll let Dr. Dias talk about this study. So this is the data that we have already communicated from our completed study. We showed this data at ASCO GI last year, 2025 again. And what we did was we added on in our initial program, Casdozo, to the current standard of care, Atizo and Bev. And these are the top-line data that мы showed. And what мы showed was a 38% overall response rate for context. context. Atizobev alone in Embrave 150 has given a 30%, 30, 30% ORR. We also showed a complete response rate of 17%. Again, for context, Atizubev in Embbrave 150, 7.7%. Of course, these are cross-trial comparisons, so bear that in mind, but nevertheless pretty encouraging in terms of we saw pfs was 8.1 months the activity that we sure saw was irrespective of etiology so we saw activity both in viral as well as non-viral disease which is important for geographic applicability and then the safety profile was very consistent with the teso and the bev alone what we see on the right side of the chart here then is the durability the spider plot shows that 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 CasDozo. So we look forward to seeing the data with the ongoing trial which I show you here. This is the ongoing trail and what we've done here is essentially we've swapped out Atizo for toripalamab. So we are progressing a three-armed study now. Two doses of CasDoZo in combination with toribev. which is intended to provide data to help with Project Optimus. And then ARM-C is Tori Bevelone, 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, IL27 level expression is very prevalent in these barrier tissues, like lung and liver. In terms of the current standard of care, that is a teaser bev so um i've talked about some of the benchmarks there that we are um we're looking at but again we anticipate that the benefit here will be mainly in terms of durability so we're really waiting for this data to mature the um the the the trial has completed crawl it is a multinational trial based in asia pac as well as in the us and excited about um the data to be to to mature further and we anticipate data um towards the end of this year um as we as the data does mature so i'll end here by passing it back to denny thanks rosh um so let me just let me just summarize briefly where we are with our development programs as dr dyess briefed you uh tag motiku we have six indications uh going forward i like you know most of those we'll get to this year, some next year. We're getting the initial data now. We started to talk about the head and neck study. I think it's very interesting with the data with the CCRE positives, and particularly in head and back, which is the HPV positive. We look forward to the other readouts. We also look forward at Casdoketog, which I think has particular potential. What I really like about this particular asset, though, is while Tegmo and Ketog 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 IELTS 27. And lastly, Loctorsi, 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 for the other assets in the pipeline. Thank you very much.