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

Afternoon, everybody. Thanks for joining us here for the next session. Really pleased to have Coheros with us. I'm going to turn it over to Danny to make some opening comments, and then we can jump into Q&A.

Thank you very much, Matt, and thank you for the opportunity to speak at your conference this afternoon. So Coheros is about the business of overcoming immune resistance in cancer, and we do this, I think, with three of our products, which are very interesting. First of all, of course, we have a next-generation PD-1, a Torpalmab brand name Lactorsi, which we launched into NPC, which is moving along quite well. This has demonstrated differential activity against Catruda in a number of settings, and I think primarily the NPC market has shown some very strong six-year survival data there and good positioning on the NCCN guidelines. However, in terms of the pipeline, we're very, very excited about Tagmo-Ketug, which is a CCRE-driven TREG depleter. Again, very focused. Treg depletion is a fundamental mechanism of action to help overcome immune resistance. Tregs, as we'll talk about in just a moment, proliferate upon the destruction of tumor cells with a number of mechanisms. And it is supposed that if you are able to get rid of these Tregs selectively in a tumor microenvironment, then the anti-tumor response of T cells can be restored. And then the last product, which I like a lot, of course, is Casdozo-Ketug, which is an anti-IL-27. We're moving that forward in first-line hepatic cellular carcinoma. IL-27 was discovered by Chris Hunter Penn as a fundamental mechanism for stopping immune response in barrier tissues, such as liver and lung and so on. We'll have a little bit more to say about that. Importantly, though, after two, three years, after moving these things forward, This half of the year now is very exciting. We're getting ready to turn over our data cards on a number of these studies. We have six different tumors under investigation with our Treg depletor, TAGMO, and, of course, we have the HCC study going with Casdozo. So we're happy to answer any of your questions around that. But I think it's an eventful time, a bit stressful watching data evolve, but we're having fun with it.

Great. Wonderful. So maybe we can just talk a little bit about your commercial program, and then we'll hop into the pipeline. But he just sort of, for everybody's benefit, talk about how big you think that product can be and obviously sort of, you know, from a business standpoint, what that provides, you know, for you as you're developing the pipeline.

I think it's one of the key differentiators of Coheris as an innovative oncology story that we have a commercial product that's out in the market launching and making money. So we're approved in nasopharyngeal cancer. We are the only available and approved therapy in the U.S., the only guys out there selling. It's about 2,000 patients a year. This translates to about $250 million in opportunity. We estimate that we'll probably be able to reach about 70% of that at maximum market share. That's perhaps $175 million per year. We've been marching that product up. Last quarter, we did 15% quarter over quarter, which was pretty strong. We certainly won't do that every quarter, but we were happy to see it last quarter. Last quarter, I think we did about $13.6 million in sales. When we get to about $15 or so million in revenue from that product, the cost of the commercial team, the COGS, the royalties, and all that will all be taken care of. So any sales beyond $15 million a quarter, we start to cover the overarching SG&A of the company, which, of course, is our focus. We project that next quarter, probably in the second half, Q3 or Q4, that will reach 30-plus per quarter with that product. I think that's a reasonable rate to achieve. At that point, the SG&A and the core burn of the company, the clinical trial costs will be covered. So that will be a big deal for us in that we won't have to keep going back to the market just to keep the lights on and so on. We've reduced the size of the company over the last three years to about 140-ish people from a max of about 360 as we sold off the Lucentis biosimilar or the Humeyra biosimilar, et cetera. So we've got a nice, tidy little innovative oncology company here with a very well-controlled burn. So as I indicated, about in 2027, we'll get to 30-ish plus and have the burn covered. And then ultimately, I think, in 28, somewhere along there, we'll be able to, I think, hit a plateau on a quarterly basis. So, you know, that's like 40-plus per quarter, so there's a little extra to cover things that come up here and there. And then I suppose in 2029-ish, we'll actually get up to where we max out for the year. But we're projecting 150 to, say, 200 sometime in that general timeframe between 28 and 29. And I think that it gives us considerable operating latitude. The challenges that we have in the market there is that Keytruda has been used in head and neck cancer for a long time. And these are the same physicians that are treating nasopharyngeal cancer, even though with respect to etiology, it's a much different cancer. So there's an educational process upon which we show them the six-year survival data, which is over 65 months versus chemotherapy, which is 33-plus months, something like that. We show them the six-year survival data, the NCCN 1A guidelines, and so on. And it's an educational process. We find them responsive once we show them that, but we do have to do that convincing. And so we're very focused this past year on, first of all, binding enough data to where you understand who all the physicians are and who's writing the scripts, understanding where we're missing the scripts, and then focusing the team in a sort of multiple disciplinary fashion to block and tackle our way through that. So that's the lift that we're doing right now on that, and you'll get more updates on that as we go forward this year. The interesting thing, though, about having your own approved PD-1 is two- or three-fold, actually. First of all, if you go to do clinical trials, you're not buying drug from other people. You have a proprietary PD-1. And as we pivoted the company strategically, that was one of the things that was most important to us to have one. Secondarily, we're combining that with both Tagmo-Ketog, the NTCCR8, and Casdozo. So ultimately, if those are approved, we'll get an additional label indication approval for Lactorsi for each of those indications and sell two vials, two moieties for each sale. So I think that's actually a very efficient way to generate additional sales and additional label indications in the future. I think that's a differentiated story. I think that there's a challenge of overcoming the contributor resistance, but we're up for it.

Okay, great. And then maybe just one other commercial question, just would you think about adding additional commercialized products into that sales force that you've built to gain additional leverage?

Yeah, absolutely. I think that once we get a little further on with the progress in the MPC, we'll have bandwidth to do that. We continually monitor developments in the market for additional products. We looked at a couple last year, for example. I think that you have to be very, very selective with particular products. Maybe the best ones are the ones that you developed yourself. But I think that we're open to collaborations and working with others and so on. But that certainly is top of mind.

Okay, great, great. So CCR8, Tregs, I think investors have heard a lot about Tregs, understand sort of the biology to a certain degree, but want to understand, you know, do you have the right Tregs? Are you going to make the right impact on the tumor? You know, what's your specific biology? So maybe we could just walk through a little bit of, you know, why you think you have the right approach here.

So certainly Treg depletion, like a lot of things in oncology, is an area of, you know, tremendous promise. But oncology by its nature, you know, very nature is a prove-me sort of area. You know, there's countless companies where people didn't think their products were, you know, going to do very well, and then they did spectacularly well. T-reg depletion, I think, has significant promise, but the issue has to be that in which particular cancers, in which particular line of therapies can its benefit be realized. So first, in that direction, Treg depletion frees the immune system and potentially reactivates the T-cells to go after the tumors. We were the first team to show remodeling of the tumor microenvironment. Last year we showed data, and they had a next study, a fourth line, in which we showed Treg depletion and subsequent infiltration and proliferation of CD8-positive T-cells. In that very same study, we saw significant diminution of a tumor. It was a 2.8-centimeter tumor in a patient's lung. So it was a head and neck patient with a lung metastasis. And we saw a diminution of that tumor. And that was really proof of concept. That happened with co-therapy with Torapalmab, so the activation of T-cells pursuant to PD-1 administration. But that was very, very exciting. Based on that data, Rosh and his team have gone forward now with a second-line study in head and neck, which we talked about on our call in August, and we're going to have a little bit more to say about next month. Generally speaking, though, I think that one has to be careful with Treg depletion and these CCL rate agents. This was the discovery that the Treg regulatory cells in the tumor microenvironment where differentially expressing CCR8 on their surface was made, you know, by Rudinsky and company in 2016, Moro Sloan Kettering. And the race was then on to try to find molecules that would attach to that CCR8 and then subsequently provide effector cell-driven depletion selectively in the tumor microenvironment. And, of course, we've done that. But this is a GPCR receptor, which is a very small piece of real estate sitting there on the top of the cell. And so it had been very difficult to find sufficiently selective agents to do that because if you make an antibody, it will cross-react with a lot of different things. As a matter of fact, we tried for two years. We were unable to make a selective antibody ourselves. We acquired service oncology, and they had screened their agent against 5,280 surface cell proteins in the genome, and they found that it only binds to CCRA, which is quite good. So we believe we have a best-in-class asset, high affinity, textbook PK, and again, we've shown remodeling and so on. A couple of the players in the field, I think, are seeing various flavors of cross-reactivity, significant fusion site reactions, or other types of side effects. In general, Raj could comment further, but in general, I think that the tolerability profile is very sufficient for us as we go forward here. But I think that is really the key, and that's why there has been attrition with respect to these CCRI agents by a number of the players in the field. But I think there's two or three players, though, that probably have decent molecules that are going to go forward, and we count ourselves among them.

Okay, great, great. Well, maybe we should talk a little bit about the trials you're running, the tumor types you've picked, you know, and sort of how that sequences with some of the data updates we'll get in the near future.

Sure. I'll tee it up for Raj. So, overarchingly, there's six different tumor types that we're going after, given the proof of concept that we saw with the fourth-line head and neck. The first is a second-line head and neck. We're then investigating the GI tract and a number of cancers, first esophageal, second and first-line, then gastric, and finally CRC, fourth-line colorectal. Additionally, we did a deal with J&J, and we're investigating late-line prostate cancer. So, Rashi, you want to talk a little bit about the second-line head and neck study?

Yeah, absolutely. Thanks, Jenny. So a couple of points I'll mention up front. So we do, as Denny mentioned, we have a very broad program, but one that's well supported by the biology in that all of these tumor types have pretty good expression in terms of CCR8 levels within the tumor. The second thing I'll say is that we have two protocols then that are active and a third protocol about to start. Protocol one is the second-line head and neck squamous cell program. Protocol two is the GI program that essentially Denny mentioned, which has four cohorts. It's second line upper GI adeno, it's second and first line esophageal squamous cell, and then fourth line plus CRC, and then the third protocol about to start is the prostate cancer protocol with PASRIDAMIG. Before I just kind of dive into a little bit about what we're seeing so far, I think it's important to bear in mind exactly what questions we are asking of this program, because I think they are a little bit different depending on which cohort we're talking about. For the three cohorts that are second line specific, so that is esophageal, upper GI adeno, and head and neck, we're asking the question, can we reverse PD-L1 resistance? Because most, if not all, of these patients will have previously received a PD-1. So that's a very specific question we're asking. For the first line of esophageal squamous cell cohort, we're asking, can we combine with chemotherapy, which then, if we can safely and effectively do so enables us to go earlier in the treatment paradigm and then for the colorectal cohort very late line we're asking the question can we convert a cold tumor and make it into a hot tumor right and then that allows us then to go earlier in the colorectal space and of course we're asking the novel novel question so what we've communicated so far in the second line head and neck study, the 40 patients fully accrued. At our last earnings call, we did communicate three things. First of all, number one, we are seeing an acceptable and manageable safety profile, which is very important in the context of the evolving CCR8 space. And in fact, also in terms of the evolving head and neck space as well. Secondly, we communicated that we are seeing activity both in terms of response, but also in terms of duration. That duration is very important with IO specifically because that's historically where IO has benefited, has been in extending that duration of therapy rather than purely response rates. The third thing that we are seeing is enrichment of activity, and we're seeing enrichment in two areas. Number one, those patients who are HPV positive, and secondly, in those patients who have a high expression of CCR8, So a lot of CCR8 within their tumor, we're calling that, we've coined the phrase TIRI, or Tumor Immune Regulatory Index, which is a measure fundamentally of the CCR expression within the tumor. One other thing I'll say is that with HPV positive specifically, which is where we're seeing a signal or enrichment of that signal, that is where we feel that there is significant white space. Because if you look at the EGFR bispecifics, the ADCs, et cetera, in particular, the EGFR bispecifics are being focused mainly on or their efficacy is being driven by HPV negative. So we think that's a nice space to play in, and I think our data is guiding us towards that space specifically. So more to come in October, but that's kind of a high-level summary of what we're doing and what we've seen so far.

Okay, perfect. So I guess maybe two follow-on questions for that. So, you know, we'll also likely get pedo data before the end of the year, it sounds like. So, you know, that's obviously a different pitotuzumab. So, you know, how will that data influence how you think about head and neck as a population? And then I think the second thing is, you know, as you point, some of the tumor types you're studying, right, the standard of care is fairly robust, and others, you know, like CRC, standard of care is very, very poor. So how do you think about sort of the bar that you need to see for some of these tumor types to move ahead?

Great question. So let's take two questions in turn. So first of all, PETO, yes, absolutely. But that's what I was alluding to in terms of the EGFR bispecifics. PETO in particular, so PETO is the one that is looking at both HPV positive as well as negative. But if you look at their data so far, we still feel there's white space in the HPV positive space because that efficacy so far has been driven really by HPV negative. The second thing is the durability is hugely important. And I think, you know, I emphasize the importance of durability, but one of the key reasons for that is that is really what matters from the patient perspective. They want to live longer. It's also the approvable endpoint, right? So you don't get approved on response rate. You get approved on survival, PFS, durability, essentially. So I think that's the second point. And then the third point is there's a significant amount of toxicity. So if you speak to some of the KOLs, they will say the toxicity really needs to be managed for some of these EGFR bispecifics, rash, etc., etc. So I think that's where we could show an advantage, and that's also why I emphasize the acceptable and manageable safety profile we're seeing so far. So to the second question, I think, yes, we are looking at fourth line plus, as you say, for CRC. maybe earlier lines with some of the other tumor types but we are fundamentally looking at areas where there remains a clear unmet medical need again if you look at the head and neck space right now the current standard of care is cetuximab, other chemotherapies, you're looking at a response rate of 13 to 15% so the bar at least in terms of response as well as duration, I mean the PFS is about two months is pretty, you know there's a lot to be improved upon and that's where we are hoping that we can help.

As Russ indicated, the KOLs we've talked to believe that the etiology of PETO and the other EGFR-driven bispecifics is primarily in the HPV-negative space. And what's interesting with the data that we've looked at so far, as we indicated in our call, is that TAC1-ketog appears to be working much better in HPV-positive, and there appears also to be an opportunity to select patients on the basis of CCR-8. And so I think selectivity in those two dimensions is something that we'll take a look at after we turn over the rest of the data cards and look. But I think that presents the opportunity, I think, for having a better impact on patients. Got it.

Okay, helpful. And then I guess the last thing maybe on CCR-8 is, so could you just talk a little bit about the plan from here, so you'll get some of this data in, you know, and this is sort of what I was alluding to in the prior question, how are you going to make decisions on what you do next from here, and do you need the whole cohort across all of these tumor types, or might you take data from, say, head and neck and decide on a path forward alone with that?

Just to rotate that, that's a great question, which is, it's just difficult to answer in the absence of data, but I'll answer the hypothetical regardless. I think, first of all, as Rasha indicated, we're going to develop a very good understanding where Treg depletion can be efficacious. You know, what is the immune context of each of these and what can go? I think what's very, very interesting about Treg depletion is its ultimate compatibility with some of the other therapies. You know, ADCs, KRAS, radiation, you know, VEGF, these tumor-killing modalities all generate Tregs. So, therefore, it's the combinability. So, we don't really feel that we're going head-to-head against PETO, right, or we're going head-to-head against KRAS. You know, we see that as a synergistic mechanism of action whereby the ORR generated by these therapies can have the adjunct of duration added by TREG depletion. So that's ultimately where we're going. So it's not really how we have to beat them on ORR out of the gate. It's how we combine. It is true, though, that we are combining now with our PD-1 so we can understand the activity of T-cells and restoring the immune response. But we fully expect to continue to have partnership combinations, as we did with J&G, with T-cell engagers, right? A T-cell engager needs a T-cell to engage. And if there's not one in the tumor microenvironment because they've been excluded by Tregs, you know, that's an issue. So that's why they're very excited. All that being said, I think that would be very interesting across these tumor types, these six different tumors that Ross is investigating, to see how the presence of CCR8 and the signal are correlated. And I think that would be very interesting. So if we see consistency, for example, from CRC and esophageal and gastric and so on, and even head and neck, and we understand how we can follow this, I think that lends more credibility to that targeted therapy. And I think that's what's particularly interesting for us. That said, we have to also keep in mind, though, that these are early-stage studies. These are phase one studies. They're not really controlled studies, single arm. So we'll have to follow up with the appropriate Phase II program and see what's very promising and where you can roll into a pivotal.

Okay, great, great. So maybe we should switch to IL-27. I think, as you referenced, the biology there is known. I guess the question is, how did you pick the tumor types that you think made the most sense, and how do you think about differentiation with your molecule?

Yeah, let me cover the mechanism of action for just a bit, but then I'll let Rush talk about the basket study that we did. So IL-27 is quite interesting. It's actually one of my favorites because it's a very straightforwardness of the mechanism of action. IL-27 is in barrier tissues. It's responsible for turning off the immune response subsequent to invasion. And it does that in three ways. It first upregulates all of the checkpoints, PD-1, LAG-3, and all these different things. Secondarily, it downregulates the expression of all the inflammatory cytokines, interferon gamma, and so on. And thirdly, it turns off a natural killer cell response. So this is a very, very powerful response. In the knockout model, as you might recall, when you knock out a rodent with IL-27 and then you give them a pathogen as an insult, the body will respond and deal with the pathogen and resolve it, but the immune system does not turn off, and the animal dies of autoimmune disease. So this is quite interesting. What we did is we did a basket study across a number of cancers. And Rash, why don't you just update on how that came out and how we got to the indication selection?

Yeah, so as Denny said, IL-27 is expressed significantly in barrier tissues, right, such as liver, lung, and renal. So our initial study, our initial phase one study, did include those three tumor types, and what we saw was responses actually in those three tumor types, some as monotherapy, some as combination. So following that, we did move into first-line HTC, with obviously there's potential to move outside that, but our initial area for exploration based on that initial study is first-line HTC. The study that we've presented so far that is complete, we presented at ASCO GI last year, 2025, and what we showed was a pretty impressive 38% ORR and a 17% CR8. So the study was Casdozo added to the current standard of care, which is Atizobev, single arm, just adding to the standard of care. So I mentioned 38%, what Atizabev alone has given is 30%, and also I mentioned a 17% CR rate, what Atizabev alone has shown is 7.7%. So again, bear in mind, these are cross-trial comparisons, so they're not exactly like-to-like, but nevertheless, I think very encouraging to see double what Atizabev alone has shown in terms of CR. There was also very good durability, a couple of patients out in CR for a couple of years, and the PFS was 8.1 months, which again beats what the current standard of care does. Safety was pretty good as well. There was no added toxicity over and above the toxicities of atezobevolone. So based on that, we've moved on now into the study that we're doing, but that was essentially the rationale for the initial tumor type selection, and our initial focus is first-line HCC, we have the potential to expand into additional tumor types as well.

What I like about the Kezdozo program is we're on the follow-on study already, whereas with the Tegmel program, all well and good, but really they're single-arm studies. They're not controlled. Kezdozo has two doses of Kezdozo, high and low, together with Toropel, Mab, and Beb, versus Toropel, Mab, and Beb alone. So you'll be able to see the IL-27 response. You'll be able to see if there's a dose response, and you'll be able to see if the duration really pans out. So I think when we get done with this study, while it may take a while to see that duration develop, you know, over the various scans, we'll be able to understand if it's indeed IL-27 driven. You know, we've got a good antibody for it. We can assay for it. And our conversations with the KOLs lead us to believe that they would be very welcoming of a targeted therapy where they could select the patients. So it's a question of how many of these patients. But this is first-line liver, so this is a very nice indication. It's a huge unmet need. The other thing that I would say about CasDozo is it's very, very safe. There doesn't appear to be a lot of adverse events. It's very much just like using a Teslobev itself. So, you know, that's a very nice thing in cancer to have something with very modest side effect profile. But I'm pretty excited about it. I think the other thing from an investor viewpoint, just to diverge for a minute, what I find interesting about it is the balance and the diversification that it brings to the portfolio. You know, so on the one hand, Kazdozo is highly focused, very nice indication, very sort of clean biology that you can test, you know, a biomarker, you know, right down the road. And on the other hand, Tagmo, although I suppose you could argue it has much broader potential clinical utility across a number of cancers and combination therapies and lines of therapies, very, very large, revolutionary, you have that inherent balance for your investors, and I find that very attractive.

And obviously you're going to need that data to mature with a larger study, et cetera. Can you just talk about how you're thinking about the timeline for that data set?

Yeah, absolutely. So let me just reiterate the design that Denny was just talking about because, again, I think it's important to bear in mind what the aims are of the study. So it's 72 subjects. What we've done is we've swapped out TORI or swapped out Atezo for TORI, two doses of Casdozo in combination with TORI-Bev versus TORI-Bev alone. That enables us to do three things. Number one, first of all, characterize safety and efficacy with a higher number of patients. Number two, it allows us to get some data towards Project Optimus with those two doses of Casdozo. Number three, it allows us to get data towards contribution of components with the Toribab arm alone to see what Casdozo adds on top. That's what the study is. That's what the aim is. So we completed a crawl to the study around March. We are now just waiting for that data to mature. What we anticipate is that the initial effect will be due to VEGF. So that will be the VEGF effect that initially causes that response because, of course, HCC is a very vascular tumor. Vascular remodeling happens quickly. And then we anticipate that durability to be, again, with Casdozo, which is actually what we saw in the first study as well.

Go ahead. I'm sorry. I was just going to follow up from Rush's remarks because you asked about the potential pivitals. The other attractive thing issue with Casdozo in terms of follow-on registration study is you're basically going on top of standard of care, which makes it very, very straightforward and very easy. I would like to be in that same situation with TREG depletion and TAGMO and KTIG where if you look into a second line or a first line indication and somehow you can go on top of standard of care, I think that's a better bet and a good spot to be in.

Yeah, yeah, yeah. No, very, very helpful. And I guess the last question here was just remind us on the, you know, in terms of development of the CRs that you saw in the initial study. So they obviously took longer to convert some of those. Exactly, yeah. That's why the durability here is going to happen.

Well, exactly. Yeah, I think that's exactly what I was going to say, that basically the durability will take time to mature. So as I said, the trial completed accrual in March. We're just waiting for the sufficient number of patients to have had a sufficient number of scans in order to see, you know, to make a good judgment about the data. When that happens, we will communicate that data.

And the point that I would make with that is that that's entirely analogous, you know, to what was seen when PD-1s first came to the forefront, right? You had chemotherapy, then you had chemotherapy plus the PD-1s. And where you see the benefit is not, you know, early in the response, you know, with PD-1 treatment. you see on the tail, just like with toropelumab, right? You know, 67 months of response, you know, survival versus 33, 34 months just on chemo alone. So you see that at the tail end of the curve, and the patients are living longer, and that's the approval endpoint. So, you know, that's how, you know, taking care of the immune response works. So we'll have to wait for it a bit.

Matt, I'll just make one last comment to your question. The other thing that we are looking at with the study is biomarkers, of course. So we'll be looking at based on IL-27 levels, but also CT DNA as well. And that could be actually an early indicator of activity as well as level of baseline disease.

Perfect, perfect. Maybe just to round us out, obviously you're a biocheck company. Cash is an important component of the business here. So how are you thinking about your runway? How are you thinking about your...

Well, you know, the one thing about being a public biotech company is people have very good visibility into your cash and your burn most times. I think we do a really good job with our cash and managing our cash and going forward. I think we're very good with our organization, which is, I think, highly effective and very, very highly integrated. You know, there's additional pieces of cash out there, for example, milestones. you know, from our partners that are lying around and a few other things. But we focus on that quite a bit. We're very cognizant of that. You know, ultimately, our strategy is to drive the company to SG&A break-even on the back of Lactorsi at the end of next year, you know, bridge that with the required cash. And then I think if you go to the investors with the case that, look, you know, here's the data, here's the study, they can vote with their wallets. And I think that's really what you have to do. And the investors that we have talked to, though, when they look at our studies, particularly, you know, like the Casdoza study where it's controlled and so on, you know, I think they view that favorably in the feedback that we've gotten from investors on how we are proceeding with Tagmo-Ketug and understanding the biology of T-reg depletion is very, very positive. You know, we're not out there just, you know, throwing mud on the wall and trying to understand what's going on. We're very systematically working through a number of cancers, a number of lines of therapy. We're looking at all the biomarkers. We're characterizing the immune environment. And so I think that's very thoughtful drug development. Great. Wonderful.

Great to have you both here.

Thank you very much, Matt.