Coherus Oncology, Inc. (CHRS) September 2026 Conference Transcript

Welcome to the Baird Healthcare Conference. Really excited to get things kicked off today with Coheris Oncology. The management team here to my left are going to do a presentation, and looking forward to hearing the exciting story ahead.

Thank you, Brian. Thank you. I'm Denny Lamp here. Coheris is 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, Tagmonketog, Casdozo Ketog, 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 of paradigms. We'll spend a moment talking a little bit about overcoming immune resistance through T-reg the patient. Of course, you're aware that we have a product, Tagnol-Ketog, which is in a number of phase 1 and 2s, 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 casdoketoid, which is our first in-class IL-27 antagonist, which is in first-line liver cancer. Coerce Oncology is focused primarily in the arena of overcoming immune resistance. The post-administration of most chemotherapy agents, the cell type called T-regulatory cells developed, so 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 marketed product. I will prize 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, tagging with TTOG. This is a CCRA positive T-reg 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, BMS 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. 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 the static prostate cancer. Casdozo-ketug 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'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 PD-1 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 Lactorsi. Lactorsi 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 Cotrida. 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 lactose plus chemotherapy versus chemotherapy alone, and this profound efficacy has been rewarded with top positioning on the NCCM 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 electorsi in the nasopharyngeal space. This is about a $250 million opportunity all in and 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. Now, 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, royalties to our partner, and so on. So therefore, well, revenues 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 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 cost. So our objective here, then, is to finance the company with the core of burn 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, you know, $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 Catruda, which has been entrenched in the market prior to our launch. Catruda has broad utilization in head and neck. 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, 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 Locturzi in the pipeline is both as a revenue generator in the context of Mesofranchio, but also revenue multiplier. So whenever any of these indications with either Tegmo or Ketog or Casdoso or Ketog are approved, we will register a sale both for that novel asset and Locturzi. Let me talk a little bit about overcoming immune resistance through Treg depletion. Tregs are immune-suppressive T cells that support immunostasis. 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 were 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 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, right? 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 CCR8, 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 Tregs in the periphery versus the tumor microenvironment. 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 TRI, 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 CCR8-derived index. It is very much akin to what you see, for example, with the PD-1s, you know, with the CPS score. You have to have 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 TAGMO, how it is differentiated from the other assets that are out there being developed by various companies and so on.

Thank you, Danny. So TAGMO-ketog is our CCR8 targeting antibody, and we believe, as Danny 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 5,500 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 the 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, pre-treatment, 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 CD8s, coming in as well. When we added in toripalumab, and you see this panel on the right, when we added in toripalumab, 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 patient. So this is a patient who previously failed a PD-1, previously failed a taxate, 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 which will have its first cohort as that prostate cancer protocol that, again, Denny was alluding to, third-line-plus population in combination with Paziridamig. 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 esophageal squamous cell cohort, we're 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're looking at essentially, can we turn a cold tumour 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 a 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 type 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. um so let me just say a few more words about the head and neck cohorts specifically which we did talk about at our earnings call um a couple of months ago um so this is a further expansion as i say of um 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 tori palomab 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. But 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. And then 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 TRI 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. Many 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 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 contributory. 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 at 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, Rush. Just before we leave the Tegmo-Ketug, perhaps you could just comment briefly on the side effects and the tolerability profile that we have seen with Tegmo-Ketug 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. And what we've seen 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 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.

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 PASRIDMIG. PASRIDMIG is J&J's T-cell engager. it has shown in some encouraging early data in metastatic castrate-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 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, 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 Casdozo-Ketug, 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 an 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, okay, you know, secondary to pathogen invasion, and it does this really in three ways. It first upregulates these various checkpoints, LAG-3, B2-1, 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. And the other thing, 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 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 These are the top-line data that we showed, and what we showed was a 38% overall response rate for context, ATISO BEV alone in BRAVE 150 has given a 30%, 3-0, 30% ORR. We also showed a complete response rate of 17%, again, for context, ATISO BEV in BRAVE 150, 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. And then the safety profile was very consistent with the TISO and the BEV 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 Casdozo. 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 a TESO for Toripalamab. So we are progressing a three-arm study now two doses of casdozo in combination with toribev which is intended to provide data to help with project optimus and then arm sees toribev 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 il27 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 TISO-BEV. So I've 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're really waiting for this data to mature. The trial has completed a crawl. 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. So I'll end here by passing it back to Denny.

Thanks, Rash. So let me just summarize briefly where we are with our development programs, as Dr. Dias briefed you. Tagmo and Tiku, we have six indications going forward. Most of those we'll get to this year, some next year. We're getting the initial data now. We started talking about the head and neck study. I think it's very interesting with the data with the CCRA positives, and particularly in head and neck, which is the HPV positive. We look forward to the other readouts. We also look forward to Casdo-Keytug, which I think has particular potential. What I really like about this particular asset, though, So while TAGMO and KITUK 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, LOC-TORSI 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.