Good morning, everyone. Welcome to the Jefferies Global Healthcare Conference. My name is Max Meier with the Jefferies investment banking team. I'm proud to welcome Denny Lanfear, CEO of Coherus Oncology.
Thank you, Max, and thank you to Jefferies for the kind invitation to today's conference. Let me first apprise you of the company's forward-looking statements and direct you to the company's SEC filings to Form 10-Q and 10-K relevant to the products, particularly LOQTORZI and so on. Today, I'm going to talk about a few subjects for you. As you know, Coherus Oncology is focused on overcoming immune resistance in cancer with tagmokitug, our CCR8 Treg depleter, and also casdozokitug. Today I'm going to give you a brief recap, first of the company and our strategy. As you know, we divested our biosimilar business some two years ago, and we've been a full-on immuno-oncology company now for a year. I'll talk a little bit about the company's overarching strategy, which includes, first of all, LOQTORZI as a backbone PD-1.
This is a commercial product, of course, which is generating sales. It's on a nice escalating ramp going out into 2028, when we project we will achieve $175 million run rate per year. I will take a moment really to talk a little bit about a very interesting topic which has come to the fore, which is CCR8-driven Treg depletion, the roles that Treg plays across cancer and across therapies. I will just drive down a little bit and I'll talk about tagmokitug and why we believe tagmokitug is the best-in-class CCR8 Treg depleter, how we are proceeding with that and its implications for our overarching strategy. Lastly, I'll spend a little time on casdozokitug. As you know, we have a first-line HCC study that's going forward in conjunction with LOQTORZI.
I'll give you an update on that, a projection of when we're going to take a look at the data and how the enrollment so far is going. First of all, our focus at Coherus, as you know, is on value creation through drugs, data, and deals. As I just recapped for you, we have LOQTORZI, which is a commercial PD-1. Importantly, though, we are combining LOQTORZI both with tagmokitug and casdozokitug, two products which we have global rights. We're doing seven or eight studies, different arms, with tagmokitug and CCR8 across gastrointestinal cancers, including CRC, but also head and neck cancer. Then, of course, casdozo, as I just indicated, with liver cancer.
With respect to the deals, as I indicated, we have global rights to these products, so we look forward to doing global deals with each of these products as we go forward and generate the data with ex-U.S. licensing. We've already done a number of supply agreements with LOQTORZI earlier phase. We look forward to doing later phase products as an efficient way to expand the label. Lastly, though, what I'll spend a little time about is tagmokitug with novel combinations for third parties. This is our pipeline slide, which you've seen. As you can see, each of these studies is in combination with LOQTORZI. LOQTORZI, in the context of our strategy, is both a revenue generator with NPC and also a revenue multiplier. As you also will note from the chart, we look forward to turning over a number of data cards this year.
We are addressing a potential of $33 billion in product opportunity with these various studies. This is because our strategy is to combine these novel products in the pipeline, casdozo and tagmo, with toripalimab. This is two-for-one label expansion with the products, and the opportunity to expand even further ex-U.S. Let me talk a little bit just briefly about LOQTORZI before I move on to the pipeline. LOQTORZI is a next-gen PD-1 inhibitor, which has demonstrated differentiation both in vitro and clinically. It is significant because it actually binds to what is known as the FG loop with PD-1, which causes subsequent internalization and has a differential effect on T cell activation, which we've seen. There's actually a nice publication on this in which we compared it to pembro.
As you can see, it has very high affinity. We've also shown in that paper that it has differential impact on SHP-1, SHP-2 signaling, which bodes well for its other activation. Clinically, though, is where things really get interesting. As you can see here, LOQTORZI has demonstrated that it's active in low PD-L1 states, particularly here, as you see in esophageal, where the hazard ratio is very similar to that in high PD-L1 states. You could contrast that on the very right part of the slide, where you see KEYTRUDA with a much higher hazard ratio in these particular cancers with high PD-L1. Indeed, LOQTORZI is actually approved in the EU for low PD-L1 esophageal. LOQTORZI also has demonstrated significant patient benefit clinically. Here you see the six-year survival data.
These patients went from 33.7 months on chemo alone to some 64.8 months on a combination of chemo plus LOQTORZI. These patients are living almost twice as long. This product has earned top billing on the NCCN guidelines. It is the only preferred regimen established in the NCCN for nasopharyngeal first-line cancer. Our commercial team is highly focused for 2026 to deliver on the growth of the product, as we have discussed earlier. First of all, the six-year survival data has been very well received by the healthcare providers and the physicians. We were just at ASCO this week, and I think we had some 38 meetings with KOLs. I attended at least a dozen of those myself. I think this six-year survival data will really put us in a strong position to drive sales and patient benefit over the next couple of years.
This year, we've also purchased more data, greater claims data. What this allows us to do then is to understand who's writing scripts, where the patients are, and then have very targeted educational promotional programs. We've dovetailed that with two other things. Enhanced information systems, so the field can go out when they get an alert, and they'll know where the patient is. They find the doctor, then they deliver the message. Also, broader field input. We've increased over the four regions. We've increased two additional people per region. We've gone from four to six in order to be able to deliver that message in a better way. Also, dedicated veteran affairs team and then an internal salesforce team. This gives us confidence that we'll reach two key metrics that we've talked about.
First is a $15 million per quarter this year, and secondarily, $30 million-$35 million per quarter sometime in 2027. Lastly, a run rate of $175 million in 2028. Let me talk a little bit now about our CCR8, and I'll start with a little biology lesson on CCR8-driven Treg depletion and why we think this is a potential new scaffold across solid tumor therapies. As you may know, CCR8 Treg depletion is coming to the fore. This is an area which has been active for some time. CCR8 Tregs are present in cold tumors. They preclude having active CD8+ T cells. You can see here a map of the various tumor types. We are pursuing the ones that you see in the red, CRC, gastric, head and neck, and so on. You see two things here.
First of all is the volume of CCR8 Tregs, and secondarily, the percent of the Tregs that are CCR8 +. What T regulatory cells fundamentally do is they moderate the immune system. They moderate the immune system turning on and off. Cancer uses this moderation to grow and to proliferate tumors. When Tregs are abundant, what that means is you do not have CD8+ T cells in the tumor microenvironment, and the tumor grows. There's long been posited that if one were able to differentially and selectively deplete T regulatory cells in the tumor microenvironment, then you would be able to have CD8+ T cells go after the tumor. Indeed, we've shown that. However, in the broader picture, what's very interesting, I think, about Treg depletion is the role that it potentially plays across various therapies.
As it turns out, cancer therapies that are cold result in the proliferation of Tregs. This is a natural wound-healing mechanism. Radiation, I'll talk about this, I have a slide that will follow in just a moment, but radiation and chemotherapy and ADCs proliferate T regulatory cells. T-cell engagers cannot be effective without the presence of CD8+ T cells, and those are precluded by existence of T regulatory cells. Targeted therapy, and particularly anti-angiogenics. I don't have time to go into all these MOAs today, but fundamentally, damage to tumor tissue from any of these treatments results in Treg increases. Treg, if you're able to deplete them, this has the potential of extending survival. People get very excited about very impressive ORRs, right? You can't get approved on ORR.
You get approved on overall survival, on delivering a step change in survival to those patients. What is really, really interesting is subsequent to the first treatment, you will see this very impressive ORR. We believe that Treg depletion can play a key role on the tail in driving longer survival, and therefore has the potential to be used broadly across a number of therapies. Indeed, this is our strategy as a company. Let's talk a little bit about radiation therapy. Radiation is really a huge opportunity because 50% of all cancer patients in the U.S. receive radiation therapy, right? Radiation therapy results in more Tregs because they are relatively resilient to radiation, right? This ablates the tissue, but the Tregs remain. This is very interesting. In the bottom here, I'll show you, this is a little animal model.
What you see, might be a little difficult to see, is you can see that the very top line that is the highest blue line, this is radiation with PD-1 and with a CCR8 depleter, right? Remarkably, just PD-1 does not work very well, just CCR8 alone very well. When you combine these two, you have greater overall survival. This, I think, is very strong rationale for us to go into radiation, and we're currently looking for partnerships in which to proceed with this. The most exciting thing we've done so far, though, is the T cell engager space. As you may know, T cell engagers are very interesting. They grab part of the tumor, then they grab a T cell, they bring them together. They've been highly efficacious.
A lot of people are moving these forward. We just signed this deal with J&J recently, a few months back. Tagmokitug is now the first anti-CCR8 to be used in combination with the T-cell engager and is the very first to be used in prostate cancer. We're very proud to be doing this and be working with our friends at J&J. We're going to be spooling the study up this fall, getting it going, and see some data late in the fall or in Q1 of next year. This, I think, does a number of things for us. Number one, this validates what I was just talking of, that Treg depletion is broadly applicable across therapies. Secondarily, that tagmokitug is a potential best in class. J&J chose us. They could have chosen a number of different Treg depleters.
I'll show you in a minute why we think we have a superior molecule, but we're very proud to be working, and we think this has potential, really, to expand to other T cell engagers. Let me talk a little about tagmokitug, our CCR8. First of all, let me talk about the target. A very proficient, probably the most competent drug development scientist that I've ever run into, once said to me, "Right molecule, right target." This is where we're focused. First, I'm going to talk about the right molecule. CCR8 is a GPCR. There's not much real estate sticking out from the T cell. Very difficult to find a selective antibody for this. Many have tried. Our own efforts screened a number of these moieties. Selectivity, as it turns out, is really everything.
You don't want cross-reactivity because this is going to have impacts, for example, with side effects, PK, and a number of other things. tagmokitug, we believe, is best in class because we have demonstrated significant depletion of Tregs in the tumor. We have demonstrated strong immune modeling. I'll show you that data with the infiltration of CD8+ T cells. Highly selective. We are the only known totally selective CCR8 molecule. Lastly, strong affinity, great pharmacology, and great potency. There's been a few teams coming forward with their data recently. I included this slide to give you a little background on things as this field evolves very rapidly. This is something that we've been talking about for about two years, according to what would happen.
The first point that I would make is if you look at the very right part of this slide, you'll see some teams are advancing and some teams have parked their programs. You have to ask yourself why that is. That really has to do with the circles inside. You must, for example, first of all, have selectivity. Selectivity is extremely important. You don't want a whole series of dose-limiting treatment- emergent AEs, infusion site reactions, all sorts of problems which then limit you from going forward. tagmokitug has really, I think, scored very well in all these key criteria. The biomarker data is very impressive. The combination data that we are developing, the linearity, which I'll just show you in a moment, is with respect to the pharmacokinetics and all. This is someplace where others are failing.
If you look at their presentations, they don't come out and they don't talk about all these various things. Let me first just talk a little bit about the pharmacokinetics. This is really beautiful data. We disclosed this last year. What you see on the left side here is the doses. We went dose one to seven. We went very high on the dosing, up to 1,200 mgs. You can see we're now working on dose five and six. What's really striking about this is the textbook linearity of this PK. Absolutely beautiful. What you also see here now on the right side of this is immune activation. This is in a patient. This is patient-level immune activation. What you see, first of all, is the T cells and the Ki-67 going up, and you can see both with monotherapy and even more with PD-1.
Interferon gamma also. This really shows you that we have very strong immune activation, as one would predict with tagmokitug, particularly in conjunction with our PD-1. This was really some seminal data that we revealed last year, and this is probably one of the strongest rationales for proceeding with tagmokitug. This comes from a fourth-line head and neck cancer patient. The left side of this you see is monotherapy. You can see in the green the CCR8, and this is a paired biopsy from this patient. You can see pretreatment in the green, and below that, in the lower left, you see all the diminishment of the green, which is the CCR8 + Tregs being depleted. At the same time, surprisingly, but as one would hope, you see the CD8+ T cells infiltrating.
You can see the massive infiltration of those cells in the lower right-hand corner. This is really amazing data. We were the first folks to show this. This is monotherapy now. In this same study, we also treated patients additionally with toripalimab. Combination tagmo plus the PD-1. You see that on the right side of the slide. You see there, this is a patient that has a 2.8 cm lesion. You can see the diminishment of this lesion over the three or four scans that this patient has. Truly remarkable. It is this data that really has gotten us very excited about our program and gotten us to expand it. tagmokitug, though, has shown remarkable safety.
One of the key things that is coming up with the other programs, as I just alluded to in a moment, is some of the dose-limiting toxicities, the PK, and so on. As I just indicated a moment ago, we have seen no dose-limiting toxicities up to 1,200 mgs per dose. No Grade 3 infusion site reactions. Generally very well-tolerated, and treatment emergent adverse events very consistent with what you'd expect. This really, I think, gives us the confidence to move forward across a number of various studies. I think this is one of the key things that you must keep in mind when you look at the entire field of Treg depleters in CCR8. Once again, we believe this is driven because we have a very, very highly selective molecule, and this is why we believe this molecule is best in class.
I'll just stop for a moment and talk a little bit about what's required for efficacy for Treg depletion. You need to understand what to expect and what types of biology. What is really key about this is you must have this Treg depletion with the appropriate immune context for efficacy. Right? Three things have to happen. First of all, you need to have Treg depletion, and you see that in the top line here, in the top right panel. We have demonstrated that. Secondarily, infiltration of CD8+ T cells for activity, also demonstrated. These T cells then need to be activated, either with a PD-1 or a T-cell engager or something, so the immune response can occur. One of the ways to conceptualize the action of T regulatory cell depletion is, basically, it detunes the immune response. It turns it off.
It's a brake on the immune response. If you remove the brake, it doesn't necessarily mean the car is going to accelerate. This is why the immune context is so important when you take a look at these studies. Given that data in head and neck, we expanded our clinical program substantially. We just recently raised $50 million to help support two of these programs. All these programs are moving along on track, I would say. The first, the head and neck, which we talked about, we're now doing the follow-on study in second line. That's moving well. That's with tagmo plus tori. That is ongoing. That is almost fully enrolled, we're tracking toward our mid-2026 readout. We'll need to get three or four or five scans in, I can't give you an exact date on that, but we are generally pleased.
In terms of gastric, esophageal, and colorectal, as it turns out, the entire gastrointestinal tract is very active with respect to CCR8 and T regulatory cells. That is because your GI tract really sees everything that comes into your body, the immune response is very important. Balancing turning that immune response on and off is really important. We're doing the gastric junction and so forth, plus esophageal. I'll just remind you that we showed very strong data in esophageal in the low PD-L1 state, we're relatively optimistic about this. Two studies, one in second line, a safety study in first line. I'm personally very excited about colorectal. A number of the other players in the field are moving forward in colorectal and have seen data and so on. We're first doing non-liver mets, then we'll move into the liver met parts of this.
This enrollment is also doing well, not yet complete. We look forward to completing this towards the end of the year as projected. Of course, I talked about the J&J agreement just a moment ago with metastatic prostate cancer in 3rd line. This also, we have finished this up. The protocol's ready to go, and as we've talked about on our recent call, we look forward to initiating this in the fall. Let me just stop here for a moment and just recap a bit of the strategy that we intend to pursue with tagmokitug as the best in class Treg depleter. Our strategy is to broadly develop it as the CCR8 depleter of choice with partners and across treatments. I just gave you a brief snapshot of the rationale for why we think this is highly applicable in radiation, but also in ADCs.
We're in conversations with a number of folks that are advancing their ADCs as complementary therapy. T cell engagers. Okay. J&J, of course, as I just talked about with pasritamig, but there's a lot of T cell engagers out there, and T cell engagers need a T cell to engage with. If you have a preponderance of regulatory T cells there in the tumor microenvironment, that's difficult. We look forward to expanding those collaborations, radiation and a number of other places. A lot of the tumors where you're seeing folks advance very rapidly and getting very strong ORR these days, we think there's the opportunity for regulatory T cell depletion, and particularly with tagmokitug to come in and extend a duration for the patients. We will first define these tumor types.
This is one of the key things that we're doing now with respect to our studies and the enrichment strategies needed for CCR8 targeted efficacy. Execute those collaborations. Once again, J&J was the first one. We look forward to doing others. First do the safety trials. Then see where the efficacy is. Then finally move forward in conjunction with the companies to establish the benefit for overall survival. With that, let me talk a little bit about our other molecule, which doesn't get nearly as much attention. It's actually my favorite, which is casdozokitug. This is a first in class and perhaps only in class IL-27 antagonist. IL-27 is very interesting. A guy by the name of Chris Hunter at Penn discovered IL-27's role in turning off the immune response.
IL-27 is a very powerful moiety, and as a cytokine, it works hand in hand, of course, with cancer. IL-27 upregulates checkpoint receptors. PD-L1, LAG-3, TIGIT, everything that turns things off very, very powerfully. It also downregulates, of course, pro-inflammatory cytokines, which come out of all the T cells, interferon gamma and so on. Thirdly, moderates a response of natural killer cells. These are three very powerful complementary mechanisms in IL-27. I think that it's significant to note when you take a mouse and you knock out IL-27, the mouse can respond to a pathogenic insult, but the immune response does not turn off, and the mouse dies of autoimmune disease. This is a fundamental role, and we are the first and only ones going after this. We've done the first study here, and this is very impressive data. This is phase II.
These are the final results in first-line HCC. This is casdo, casdozokitug with atezo and bev, which is standard of care. What you see here is a very impressive waterfall plot. I think what's most impressive about this, besides the overall response rate, which is high, and the complete response rate of 17%, which is more than twice as high as standard of care, keep in mind, is the duration. There are patients, as you can see on the spider plot, on the right side of this, which go out almost two years. This really has substantial patient benefit, and again, it's complementary. This is an orthogonal mechanism of action we're very excited about. My good colleague, Dr. Dias, is proceeding then with this study. The study is now fully enrolled.
This is our follow-on study. We're combining LOQTORZI with casdozokitug and atezolizumab in this, I should say, bevacizumab here, in three arms. We're evaluating two doses of casdozokitug so we can fill Project Optimus. We're also controlling it with a tori and bev arm. I would just also anecdotally remark that toripalimab has shown very, very good efficacy in the liver studies out of China and so on. We're very confident that toripalimab itself will have very strong response. We're not concerned about replacing atezo. We've gone on. We're doing this now. This has just finished up in terms of enrollment about a month ago. We should be on track to turn these data cards over a little later as we have previously guided, depending on how many scans we need.
I would make two quick points here, though, is first of all, if you're going to go and you're going to look for duration, a one-year or two-year duration, you're going to have to wait a one year or two years to see the data. In lieu of that, we intend to do ctDNA circulating ctDNA analysis, and take a look and see if we can understand better how things are going. I think given the graph, I think we'll have a pretty good idea how this is panning out over a few months from now when we turn the data cards over. The other thing is we have one more study. There was very nice data that we saw in squamous non-small cell lung cancer with casdozo. We haven't gotten to that study just about yet. We're sort of busy with tagmo and doing a few things there.
It's something I'd like to get to here over the next year or so because that was also very, very promising. That's another area where casdozokitug could have a complementary mechanism of action. With that, I'll just close on my summary slide. As you can see, we're very busy developing tagmokitug in combination with toripalimab, but also with a number of other moieties. The note I would make to you is that we are not myopic or narrow-minded with respect to how to maximally exploit the mechanism of action and the patient benefit of tagmokitug and the opportunity to deplete T regulatory cells in the tumor microenvironment. We intend to cast our net widely. We intend to partner with others, and we intend really to see just where this will work as a function of the immune context of all the cancers that we are going after.
Casdozo, as I just indicated, the first-line liver is very good. The other point that I would make here is that casdozo has the opportunity for, ex-U.S. licensing, particularly in Asia, where there's a significant amount of liver cancer. We've gotten good interest for that, and I think as soon as we get the data readouts, we'll probably get a little busier on the deal front. With respect to the data, as I just showed you, we've gone very broadly with respect to tagmokitug across a number of cancers, head and neck, the entire GI tract, and also now prostate. We intend to investigate the immune context across these cancers, focus our programs, and understand just where we need to go for the pivotal and registration trials. Lastly, with respect to the deals, we've managed expectations there.
I think that we'll probably get things done in the six, 12, 18-month time frames, as I said before, particularly with respect to tagmo, or casdozo ex-U.S., but also with continued opportunities to exploit tagmo as best-in-class T regulatory cell depleter. With that, thank you very much. I'll be happy to take any questions