Afternoon, and thank you for joining Baird's Biotech Discovery Series. I'm Mike Perrone, Baird's Healthcare Specialist, and I'm pleased to be joined by Coherus Oncology Chief Scientific and Development Officer Theresa LaVallee and Chief Medical Officer Rosh Dias, as well as Dr. Daneng Li, Associate Professor in the Department of Medical Oncology and Therapeutics Research at City of Hope. I'm also joined by my colleague, Baird's Senior Biotech Analyst Colleen Kusy, who will be moderating the discussion today. As a reminder, Baird's Biotech Discovery Series is an opportunity for investors to hear directly from interesting and innovative biotech companies in a fireside chat format. A few quick logistics: if you would like to submit a question, you can do so via the webcast portal, or you can email Colleen at ckusy@rwbaird.com. Finally, before we begin, I am required to remind attendees to please refer to the event calendar, published research, or Baird's website for important disclosures regarding the companies discussed during this event. I'll now hand it over to Colleen to kick off the discussion. Great. Thank you, Mike, and thanks to everyone for being with us today. I'm really excited to dive in. I think a lot of investors, when they think of Coherus, are still maybe thinking of the biosimilar company from a number of years ago, but really there's been, through a series of transactions, a strong pivot now with the company fully focused on the broad immuno-oncology pipeline. So just to begin as an overview, maybe for those who are less familiar with the current Coherus story, if the Coherus team wants to kick things off with just a company overview, touch on the recent history, and now the focus on IO. Yeah, thank you for the opportunity to participate, and particularly as we look back on an important year for Coherus in 2025 and go into the end of the year and holidays. We're thrilled to be here. We're also thrilled that Dr. Li was able to take time out of his schedule to join us to give us that oncologist perspective and an expert in liver cancer and a valued collaborator on Casdozokitug program. Coherus Oncology is a commercial stage innovative oncology company with an approved FDA-approved in the U.S. next generation PD-1 inhibitor, Toripalimab, and a promising clinical pipeline. We have an experienced management team with a depth of expertise and proven success in bringing drugs to market. That's different than a lot of biotech companies that have very strong research and early phase, but not that end-to-end look. As we know, a lot of drugs get held up in the approval process for development gaps, particularly in the CMC area where over 50% of complete responses come in. Really that depth of expertise helps Coherus progress our pipeline and bring forward important molecules. 2025, as you said, Colleen, was a big year for us. With the full divestiture of the biosimilar pipeline, we are strategically focused and well-capitalized to deliver multiple potential proof-of-concept data readouts in 2026. Really to look towards those drugs, Toripalimab is the cornerstone of our oncology pipeline. PD-1 inhibitors have, we forget now 13 years post the first approvals, how much they've revolutionized cancer care. Really bringing long-term survival and even cures to metastatic cancer patients. We can start talking about treating people living with cancer versus the cancer patient. A big difference. That's why we focus on targeted therapies for the immune system to really expand to many, many more patients' immunotherapy, because even though PD-1s have been revolutionary, still a minority of patients that get the benefit. Whether our development is focused on accelerating and advancing treatments that can bring immunotherapy treatments to patients who have been underserved, so tumor types that don't have any approved PD-1 like colorectal cancer, or improving on the existing treatments. Like when we look at the Casdozokitug data that has more than doubled the complete response rate. I think when we talk about these numbers, we forget what that means. To get an overall response rate, a partial response, it means the tumor has to shrink by at least 30%. If we talked about, oh, you still have 70% of your tumor, but it's not growing, so that's good. Versus being able to say to the patient, your tumor's gone, you have a complete response. And that CR rate in HCC has shown to associate with survival. So really a big difference in adding on to treatment. Our other pipeline asset is Tagmokitug, which is a cytolytic antibody directed against CCR8. This is a protein that is highly overexpressed in tumors on T regulatory cells. So these are a suppressive cell that allows the tumor to evade the immune system. This leads to tumor progression, metastasis, and importantly, resistance to PD-1, but also therapies like radiation, chemotherapy, targeted therapy. So it really has broad potential, and the data that we've presented over the last two years from the clinical program is really showing great promise with this mechanism. Just to end with the introduction that Toripalimab is the cornerstone, so you have to think about as we advance our pipeline to do a play on words, we get a dogo, develop one, get one. It's a revenue multiplier because as Casdozo, Tori, Bev go towards approval in HCC, then that would get two drugs approved. For Coherus, we get two drugs for the development program. Then Denny will often talk about drugs, data, and deals. It's important to remember we have global rights to these assets. Deals, whether they be regional partnerships, since Coherus is focused on the U.S., so looking ex-U.S. for partnerships, as well as, as I said, the mechanisms really lend themselves to a variety of treatments beyond PD-1. Thinking of partnerships where we could look at novel combinations. So I'm looking forward to the discussion, and let's dive in. Great. That was a really helpful overview. So thank you for that, Theresa. So since we were really pleased to have Dr. Li with us today, a KOL in liver cancer and a PI in the Casdozo study, we'll spend a lot of the time today going over Casdozo, Coherus' first-in-class anti-IL-27. So maybe just to start for Theresa or Rosh, if you want to just begin talking through the target, the unique mechanism, and the rationale behind IL-27 inhibition in oncology. Yeah, because I'll give the scientific background and then let the medical folks dive into any of the clinical data. So IL-27, I mean, we forget with cytokines, right, that they're well shown targeting them with antibodies to rebalance the immune system. There's a multitude of approved drugs for inflammatory diseases. Casdozokitug is the first antibody by inhibiting a cytokine in cancer patients to show it rebalanced the immune system. So IL-27 in the right context, so cytokines aren't suppressive or activating, it really depends upon who they're around, so their environment. And what all of the preclinical studies have shown us is that when IL-27 is abundantly expressed in lung and liver, it turns off the immune system, T cells and NK cells. So that tissue specificity is really important. In all the preclinical models, we only saw activity if tumors were in lung and in three different liver cancer models. So that translated well into the clinic where we've now seen inhibition of IL-27 leading to immune activation and responses in tumor types where it makes sense. Yeah, what are those tumor types where you see this mechanism as most appropriate? Yeah, so the mouse model says when the tumor's in the liver or the lung, and it's also shown by turning off T and NK cells. And the NK cells, which is a natural killer cell, so another approach for the immune system to kill foreign cells, is really one that's been underappreciated for oncology treatments. And NK cells are rich in liver and particularly in squamous tumors. And seeing monotherapy activity in the Phase I in squamous non-small cell lung cancer really brought that mechanism through, showing that IL27 in the squamous lung in particular in these late-line patients was turning off the NK cells and preventing that anti-tumor immunity. And then even in our Casdozo clinical study, we see very profound and robust NK cell activation associating with clinical response. So really showing the mechanism in patients. Great. And so yeah, you touched on the monotherapy activity that you've demonstrated in the clinic, but maybe kind of broadly tee up for us the early data that you've shared so far for Casdozo in the Phase I study. Thanks, Colleen, and nice to see you. So we're obviously very excited about the Casdozokitug program, and we've exposed right now well over 175 patients to being dosed with Casdozo. So I think we have nice confidence in the safety profile and early efficacy as well. So the trials we've done so far, we've completed a Phase I trial, and we have now gone into hepatocellular carcinoma expansion, which I'll describe shortly in a Phase II design. So the Phase I trial initially consisted of standard dose escalation, advanced solid tumors up to eight dose levels, and we showed a very manageable safety profile with no DLTs up to those eight dose levels, and then we went on into a limited dose expansion across three specific tumor types: non-small cell lung cancer, renal cell, and first-line hepatocellular as monotherapy, but also with limited combination as well. And so what we showed, as we alluded to earlier, was some nice early activity. We showed monotherapy activity in non-small cell lung cancer. We also showed some monotherapy activity in RCC and some early combination data in HCC as well. Specifically on the monotherapy activity in non-small cell, that was very specific to the squamous cell histology. As you know, squamous cell makes up around 30% of all non-small cell lung cancer patients. And both of our responses in non-small cell was in the squamous histology in PD-1 refractory subjects and in late line, so third line and fourth line patients. So that was really nice to see the monotherapy activity, obviously rare in such late line patients. And then the HCC approach is what we've really progressed, and we can talk about how excited we are with the data that was presented at ASCO GI earlier this year as well. Yeah, great. Yeah, let's move on then to the HCC data. Some really interesting for that triple combo. And so yeah, so let's talk about the data so far, and then you can talk about kind of the ongoing study you guys have. Absolutely. So the data we presented at ASCO GI in January this year was data on the Casdozo-Atezo-Bev combination. So that is Casdozo on top of the current standard of care, Atezo and Bev. We looked at 30 subjects overall, and the population was a first-line hepatocellular carcinoma population, single arm, as I say, the triplet of Casdozo, Atezo, and Bev. And we showed some very nice responses. So the overall response rate was 38% with a complete response rate of 17%. So a couple of points in terms of context that I'll mention. So in terms of the historical controls, that compared very well with Atezo-Bev alone. So historically, Atezo-Bev has shown a 30% overall response rate compared to ours of 37%, and then a 17% CR rate for the Casdozo triplet compared to historically just an 8% complete response rate with Atezo-Bev alone. So that doubling of complete response for us was actually pretty encouraging. Obviously, it's probably the best correlate with overall survival. So very encouraging to see that. A couple of additional points I'll mention with the data set that we presented. So first of all, we did see responses irrespective of etiology. So for both viral and non-viral etiology, we did see responses. The second thing I'll say is that we saw an evolution of the results with time. So the first data cut that we showed, probably around two years ago now, showed a 27% ORR, which then went up to, as I say, 38%, and then initially zero complete responses, only partial responses initially, which then deepened to show the five CRs or 17% CR rate. So that I think was very encouraging for us to see, first of all, the responses irrespective of viral etiology, which is very important given that this is a global disease with very different etiologies depending on where you are geographically, and then also that increase in response rate and deepening of response. And I know Dr. Li was actually very instrumental in that trial and remains so to our program. So I don't know, Dr. Li, if you have any additional context you wanted to provide from your side. Yeah, absolutely, Rosh, so happy to be here with everyone, and I think as Rosh highlighted, I think the early data with the combination of Casdozo plus Atezo-Bev is really, really encouraging. I think when we think about the HCC landscape of the space, it's truly true. We've made a lot of strides, I would say, in the past five years, but as Theresa hinted as well, unfortunately, a majority of our patients don't necessarily have a response, right, so the idea is, how can we improve that, and how can we get into really deep responses or kind of that complete response where potentially these patients, as an oncologist, I never use the word remission and everything, but I'm starting to believe that these are patients that are actually in remission because they don't have any evidence of disease on imaging while out from the treatment itself. I think as we go forward in terms of development of HCC, we really require to have novel mechanisms of action, right? I think we have to go beyond kind of the traditional stances of PD-1, CTLA-4 combinations that's established in HCC. And we've already seen some early results from other studies where we just kind of combine CTLA-4 with PD-1 with Bevacizumab, and they haven't necessarily panned out, right? So that's really telling us that a novel mechanism of action approach is really required to further push the envelope in terms of development and really helping our patients with HCC. Absolutely. That's super helpful, Rosh, for the background overview of the data. And Dr. Li, for your view on the data specifically too. Curious, Dr. Li, just on safety, if anything stands out to you there and kind of how the triplet has compared to your experience with the doublet? Yeah, so I think the safety as well as potentially side effect profile of Casdozo is what's particularly encouraging, and I think it's certainly a strength of Casdozo as a partner combination to current standard of care treatments. I think what we have looked at is that whenever we add in a third agent, particularly for patients with liver cancer, this is a very vulnerable patient population, right? They have underlying liver disease, and therefore one of the first things that you want to do in terms of rational drug development is that not only do you want to improve efficacy, but you don't necessarily want to hurt the liver in these patients. Because if you do, then these patients actually get into trouble, and you're actually making the patient worse from the liver disease compared to the cancer alone. And that's definitely not what we want to achieve, right? I think what we saw in the earlier study with the triplet combination with Casdozo was that there wasn't necessarily any additional immune-related events that we would see with the third agent, which is not necessarily true compared to some of our standard of care agents like CTLA-4 agents, right? Like with CTLA-4, one of the concerns with kind of the current CTLA-4 regimens is hepatotoxicity. Many of those studies have shown that many of these patients develop immune-related hepatitis, often requiring significant amounts of steroids. And when they do that, then they might not recover as well as they were prior to the start of treatment. And I think that's what's particularly encouraging about the Casdozo study in the sense that we didn't necessarily see a significant uptick of immune-related AEs. Overall, for patients that were treated, they actually tolerated it very well, just as if they were tolerating a standard Atezo-Bev. That's great and super helpful. And so I think maybe if we can take a step back and just kind of, Dr. Li, for everybody on the line, just kind of walk us through your current practice, how many HCC patients you see, and just kind of walk through your typical treatment paradigm for a newly diagnosed HCC patient. Absolutely. Happy to share that with the group, so we're a major tertiary cancer center in the Los Angeles area, and as such, a majority of our patients that come to us, unfortunately, have advanced disease, so I would say that pretty much close to 90% of patients that I see with HCC have advanced disease, meaning that they're no longer eligible for curative transplants or liver resection, so these patients, the cornerstone is really with systemic treatment, and I think we have a very large program. We probably see close to 200 new HCC patients each year, and many of these patients, as you can imagine, at the time of diagnosis, they're very devastated with this aggressive malignancy, right, and oftentimes, that's where we have to really get excellent tumor control to offset because many of these patients are quite symptomatic. I would say that that's really where kind of in the first-line setting, particularly, this is our best shot to achieve a response in these patients, help these patients, and maintain long-term durable control for these patients. That's why I think we're really focused on kind of that first-line setting with Casdozo in combination with current standard of care. And because of those front-line patients, what% receive Atezo-Bev? Is that pretty much anybody that can tolerate it would receive Atezo-Bev? Yeah, so I personally favor Atezo-Bev just because from a tolerability standpoint, as I mentioned, compared to the other standard of care regimens in terms of combination CTLA-4-based regimens, I think the concern is tolerability in those patients and the high risk in terms of immune-related adverse events. I know sometimes in the community, it might be a little bit harder to get Atezo-Bev going just because of the EGD requirement where the patients require endoscopy prior to start of treatment for evaluation of varices, but I think if you're able to do that, and I actually would say that even in the community, no matter what, every single HCC patient should have an EGD regardless of what regimen you pick because that's the natural way to really treat the underlying liver disease and evaluate for complications of the liver disease and the onset. So if I'm going to do that as my defined standard of care, then that's ultimately not an issue in terms of getting Atezo-Bev going. And I think that has the biggest benefit in terms of overall safety as well as tolerability. And there's been recent analysis that have looked at that in terms of comparing that to other combination regimens. And they found that the combination of Atezo-Bev gave you the best balance in terms of efficacy as well as maintenance of quality of life in these patients that were treated with the regimen. When a patient either fails to respond or relapses from the front-line treatment, what's the typical next step for that patient? Yeah. So I think that's really why I said the first-line setting is really kind of your best chance to get control of the cancer and to maintain long-term durability of control of the disease. Because unfortunately, if a patient progresses on front-line therapy, our treatment options are really limited. So we certainly have the older tyrosine kinase inhibitors that we have used previously prior to the approval of the combination immunotherapy regimens. But if you look at the totality of data of those tyrosine kinase inhibitors, usually patients actually progress on the time of their first scan. So what that's really telling us is that those tyrosine kinase inhibitors, particularly in the second line or second line beyond setting, really isn't necessarily efficacious for an overwhelming majority of our patients. If essentially a median progression-free survival of anywhere from three to four months, that's usually at the time of first scan. So then it really begs the question, did it really work for these patients at all, right? So that's why it's so important that in the first-line setting that we really get this right and everything, that we give the patients really the best chance of a response and potentially a complete response where that ultimately translates to durability and the possibility of remission. You're a PI now in the Phase II study for Casdozo, Tori, which they subbed out Atezolizumab for Toripalimab, their proprietary PD-1, plus Bevacizumab. Maybe just kind of talk through your early experience in that trial so far, how enrollment has been, and just what your experience has been. Yeah. So I think there's been a lot of interest in this study and everything, and so enrollment's going great. Overall, I've been very pleased with the study, and it's been consistent with my prior experience from the earlier study with Atezo-Bev plus Casdozo. I really think that these are very comparable backbone regimens in terms of Tori- Bev versus Atezo-Bev, and maybe even potentially actually better. If you think about the data for Atezo-Bev versus the data from Asia with Tori- Bev that's been published in the HEPATORCH study, they were very equivalent in terms of efficacy for overall survival, progression-free survival, as well as objective response. I think one of the criticisms of using Atezolizumab is that there is potentially this high incidence of antidrug antibodies, right, so there's a potential kind of theoretical risk with that. Substituting Atezolizumab for Toripalimab, potentially in this Phase II trial that we're running right now, potentially erases that risk, right? So that's why I say it's actually potentially better and everything to supplement with Tori and everything where you're getting that potential similar efficacy results, and you might not have to deal with the antidrug antibodies that have been raised as a potential criticism of using Atezolizumab. Super interesting point. If it's helpful, I can just outline what the approach is that we're taking right now with our ongoing study. Please. Yeah. What we've essentially done is we've swapped out, as Dr. Li alluded to, we've swapped out Atezo for Tori. We're now looking at a three-arm study with 72 subjects, a one-to-one-to-one randomization, first-line hepatocellular carcinoma, of course. The three arms are essentially two doses of Casdozo in combination with Tori and Bev versus arm C, which is Tori- Bev alone. We're trying to really achieve three things with this ongoing study. The first one is obviously to further characterize efficacy and safety. The second is to try and address, to some extent, Project Optimus by looking at two doses of Casdozo. Thirdly, we're also trying to address contribution of components to see what the addition of Casdozo does on top of Tori Bev alone. That is the ongoing study that Dr. Lee is the PI of, and I thought it might be helpful just to kind of state a little bit of the context in terms of what we're aiming there. Absolutely. Thank you for that. And then so Dr. Li, with the helpful context from Rosh, I guess maybe walk us through the excitement for the mechanism in HCC and what you'd like to see from this ongoing Phase II study in first-line HCC. Yeah. So I think primarily, like I mentioned, whenever you add in a third agent, right, we don't want to harm the patient and everything. We need to make sure that we are actually continuing to preserve the health of our patients, particularly their liver health and everything. So I think what we want to see is continued additional safety data to show that by adding in Casdozo, this is really the ideal partner in terms of a third agent that doesn't really have any additional toxicities of our concern for our vulnerable HCC patients. And then I think once that's really established, then it's really looking at kind of the efficacy data. Are we improving upon in terms of response compared to our patients that got that's getting kind of standard of care treatments with Atezo-Bev or any of the other regimens? And then it's really kind of that deepening of the response, right? Like as Theresa highlighted, CRs are very different compared to those patients that even achieve a partial response because many of those patients that have a CR, they're going on without potentially progression for multiple years, okay? And some of them, we have not even seen progression and everything at this point after several, several years already. So this really says, have we achieved remission in these patients? And they're essentially cancer-free and everything. And for a patient with metastatic HCC or metastatic liver cancer, I could not have imagined that over five years ago because it didn't exist. So I think those are the things that are really important, and those are the things that we want to see. I think in addition to that, secondarily, like Theresa mentioned as well, the mechanism of action of Casdozokitug is very interesting. It's potentially a targeted immunotherapy approach, whereas a lot of immunotherapies are just generally broad, kind of taking off the brakes somewhat in terms of stimulating the immune cells. So I think a targeted therapy approach also allows us to potentially be able to ultimately develop a biomarker for HCC and allow us for the very first time to be able to predict for patients that are going to respond and that are not going to respond. And I think that really separates Casdozokitug from any of the other combination regimens that are in development. Super interesting. And so Rosh, for the upcoming readout, maybe just remind us the timelines for the next data we'll see for the triplet combo. And would you expect to see a dose response for the two combinations, or is that more just a Project Optimus check the box? Yeah, it's an interesting question. All of the responses that we have seen thus far have been with the 10 mg per kg dose, which equates to 700 milligrams. That's very consistent across all of the tumor types that we have seen. I think we're pretty confident in the dosing. This is really to address Project Optimus, as we said earlier. In terms of timelines, this is an actively accruing study. It is ongoing in the U.S. and Asia-Pacific countries as well. There's a lot of excitement, as Dr. Li mentioned, in terms of the previous data that were presented. It's accruing nicely. What we anticipate showing is initial data around the middle of next year, middle of 2026. Importantly, we do expect that data to mature. I mentioned earlier that the Atezo-Bev-Casdozo combination, it showed an increase in overall response rate over time, a deepening of the responses over time as well. So initial data, I think, around the middle of the year and then maturing of the data subsequent to that. Dr. Li, down the road, if this triple combination were to be approved in front-line HCC, how would you expect to use it amongst your patients? What patients would you use it in? What%? Yeah, I think that's an excellent question. And I think for many of us, I think it would be very easy. I mean, I think if this is an approved triplet regimen showing improvement compared to our current standard of care, there's no doubt in my mind that the entire community, the entire oncology community, will use this as the de facto regimen. Because like I mentioned, from a safety tolerability standpoint, this is so tolerable, and patients want that, right? And I think oncologists want to do the right thing, and they want to make sure that not only are our patients getting their cancer controlled better, but that they're actually living better, right? And that's the goal, right, and everything. So because of that balance in terms of safety as well as toxicity with additional efficacy and chance of long-term durable control, there's no question that if this gets approved, this will be the de facto regimen across the board for HCC. Super helpful. And Rosh, so you'll have the initial Phase II data in the middle of 2026. Kind of walk us through next steps would be for the development of this triplet combination? Yeah. So the next step following this would be to look to obviously an expanded design, right? So we should get the results initially around the middle of next year. Again, important to say, as I said, that I anticipate an increase in response rate and evolution of the responses in terms of deepening as well over time. The durability will be important. The totality of evidence that we're looking at will be important. But the next step following that, we're planning for a much larger Phase II, three adaptive design study looking at the Casdozo triplet, Casdozo-Tori Bev versus Atezobev alone. And again, we've talked a little bit about contribution of components in terms of our current study. We also think that we can use HEPATORCH, which Dr. Li alluded to earlier. That is, that large Tori Bev versus Sorafenib study from China, large Phase III. We think we can use that towards contribution of components. So next step, Tori Bev-Casdozo versus Atezo-Bev. Great, and so now I do want to switch gears a little bit, make sure we talk about Tagmokitug as well, recently renamed from CHS-114, if anybody's familiar with that one, so maybe first back to you, Theresa, if you kind of just talk through the rationale behind the CCR8 mechanism and how Tagmokitug is differentiated relative to some of the others out there. Yeah, now we're super excited about this mechanism and so find that the Nobel Prize was awarded to Tregs this year, really highlighting how important the cell type is. And typically, as you think of the Nobel Prize coming through, it's often when they see therapies coming. So one, adding Tregs to turn off the immune system and inflammatory diseases. And then the real challenge in oncology, because it got that recognition with the Nobel Prize because of the importance of these cells in regulating peripheral immune tolerance. So if you knock out all your Tregs, you're the bubble boy, right? So you just are going to have a rampant immune response. So that has been the problem in oncology. People have known for decades that Tregs are upregulated in response to treatment, cause resistance, cause progression of tumors, but how to selectively deplete them in the tumor and not in normal tissues. CCR8 has been that missing puzzle piece. And because it's upregulated and highly prevalent specifically on intratumoral T regulatory cells and some of the most immunosuppressive cells. So the mechanism is bind and kill. It's a targeted therapy. So we've characterized tumor types and shown broadly in solid tumors, the highest density and prevalence has been observed in head and neck cancer, gastric cancer, cervical cancer, but a very abundant prevalence and density in tumor types like colorectal, lung cancer, ovarian cancer, breast cancer, pancreatic cancer. So we're really seeing that there's a large number of solid tumors where this could really come in. And importantly, usually your preclinical data is always better than your clinical data. It's always like tickles me when it's better in the human. So what we observed in our head and neck cancer patients that were treated with Tagmokitug as monotherapy exactly does what it says it's supposed to do, deplete specifically the Tregs, CCR8 positive Tregs in the tumor. But it also brings in this large increase of CD8 T cells. And that's another immune cell besides the NK cell that is important in killing the tumor. So having them all there, so for PD1 and then in our safety cohort, adding Toripalimab to that and seeing a response in a very refractory patient really shows that those T cells are there and now ready to go. When we think about combinations, one of the things that really stood out to me when you think of other classes of immunotherapy like T cell engagers. So it binds a tumor antigen on one side, and then it tickles the T cell to activate them. Well, if the T cell's not there, it's not going to tickle it. So bringing all those T cells in, it could really be a rational combination. So super excited. And the safety profile that has challenged other approaches in targeting Tregs has not been observed to date. So we've done exactly what we set out to do and are excited about progressing this program. Gotcha. Because yeah, there have been a couple of other CCR8 antibodies in development, a number that have actually been partnered so far. I guess in terms of the differentiation, could you just kind of remind us, is it more similar than different to those, or what kind of stands out about Tagmokitug? Yeah, so from a pharmacology standpoint, there's three aspects to look at for the molecules and how they vary. The first and the easiest is, I mean, we all know from antibody drug conjugates and other things, off-target binding can lead to toxicity, right? So if you bind more than your target, so more than CCR8, it might cause toxicity. CCR8 is a type of protein called a G-protein-coupled receptor. And those are notoriously difficult to generate antibodies against. So a third of all FDA-approved drugs are against GPCRs, but only five antibodies because it's really, really hard to get an antibody that binds just to GPCR and not other proteins. So to our knowledge, Tagmokitug is the only selective molecule. And we have heard chatter about toxicity with other CCR8 programs. And that could be attributed to the off-target binding. The other aspect is I call it a cytolytic antibody because I think that's easier to understand than an afucosylated antibody. So by taking the fucose sugar off the binding domain in the antibody that interacts with the immune system, you essentially soup up the killing. So it's a supercharged antibody to bind and kill. We saw data from Shionogi's program at ASCO with a complete response and a partial response in colorectal cancer in their Phase I study. Super exciting, but their antibody is a wild type IgG1. So it's lacking that afucosylated cytolytic potency. So our molecule would be more potent than that. And we've seen some early hints of data. Like if you look closely at the data that they presented in their Treg depletion, when you combine with a PD-1 inhibitor, it activates the immune system. So it activates Tregs. So you've got more of them. They didn't show, I mean, you got to look closely at those plots. You don't see a big depletion of the Tregs in combination with the PD-1 inhibitor. And the third aspect is just simple pharmacology of where it binds on the epitope. And so a lot of times you try to block the ligand. That does cause a competition with binding. Ours is not a ligand blocker. So it binds in a distinct location. So we don't worry about competitive interference with binding to the target. So I think those three attributes really have Tagmokitug standing out as really desirable pharmaceutical properties. And we've seen that in the clinic to date. Yeah, absolutely. So yeah, so you've already generated some data for Tagmokitug and head and neck cancer, as you mentioned, Theresa. And now you're kind of taking a pretty broad development approach. So maybe Rosh, kind of walk us through the tumor types that you're going after for this mechanism, for this asset, and kind of the next steps in each of these indications. Yeah, thanks, Colleen. So we have two protocols that are running. The first one is head and neck focus. The other one is an umbrella protocol looking at multiple cohorts, different tumor types, all driven by the biology that you heard. Just very briefly, so first of all, to remind you about the head and neck, so protocol one, what we showed and the clinical data that we were alluding to earlier, we showed at AACR a few months ago data from the initial second line plus head and neck limited expansion, which we showed with out of seven patients who received the combination of TAGMU and toripalimab, we saw one partial response. This partial response, the encouraging thing for us was that it was in a fourth line patient who had previously failed a PD-1, previously failed a taxane, previously failed a TKI as well. So to see that response, such a late-line patient was very encouraging. So the first protocol now progresses that with a further expansion in second-line specific head and neck squamous cell. Protocol number two is the umbrella protocol. And we're looking at three different tumor types, four cohorts. Cohort A is gastric cancer. That is supported, I think, by some very nice data from LaNova Medicines, now Sino, out of China, which showed in the second line and second line plus setting some nice responses in terms of the combination of their CCR8 with Toripalimab specifically. So we're doing a 40-patient study looking at the Tori Tagmu combination in second-line gastric. The other area of focus is esophageal, both as a second line and a first line setting as well. This takes advantage, I think, of the activity that we've shown with toripalimab irrespective of PD-L1 levels, which is most marked probably in esophageal, so we're looking at a second line approach. We're looking also to generate some safety data in the first line with chemotherapy, and then we've also started the colorectal cancer cohort as well. We're initially looking at non-liver mets, and we'll move then quickly into liver mets as well, and as you know, this is an area where there's a huge unmet medical need. We're looking at the fourth line plus setting right now initially with a plan to move up into earlier lines where the current standard of care gives you maybe an overall response rate of around 6% or thereabouts, so a lot of room for improvement, and all of these cohorts and both studies are, again, active and ongoing. Great. And I realize some of these studies are more recently getting going than others. So maybe just kind of walk us through for 2026, what's the data we can expect for Tagmokitug? Yeah. So for head and neck, so protocol one, head and neck squamous cell, second line, we anticipate data in the first half of next year. For protocol two, where we're looking at the multiple different cohorts, gastric cancer, probably around the middle of next year, and then both esophageal and colorectal, probably in the second half of the year in terms of initial efficacy safety data. Great. So very data rich here. That's fantastic. So maybe let's make sure we touch on Loqtorzi as well, as you mentioned at the beginning, Theresa, the backbone initially approved already in nasopharyngeal carcinoma. Kind of walk us through that launch and just kind of how you're thinking about leveraging Toripalimab for your ongoing development strategies. Yeah. In terms of development strategy, I think we've covered that mainly in terms of really the backbone for both our internal pipeline, but also external providing toripalimab for development in clinical trial agreements for development with other novel agents for other companies who need a PD1 backbone. In terms of tori, we're in the post-launch period, of course. We're now a year and a half, two years, coming up to two years into launch. I think we're doing well. We're still on track to what we've communicated previously, which is a peak sales of around $150 million-$200 million in the 2028 timeframe. One thing that was very encouraging for us was at ESMO Asia probably just two weeks ago now. We presented extended survival follow-up for the JUPITER study. In the first line setting, we obviously, as you know, looked at Gem-Cis plus or minus Tori. And what we showed was with a six-year follow-up, we showed updated data showing that this very impressive overall survival advantage was maintained in the control arm of Gem-Cis alone. The median overall survival was 33 months. And with the addition of Loqtorzi, that went up to 65 months. So almost a doubling, which was very, very impressive and I think very well supported and validates its positioning on NCCN as the preferred position. So that was very exciting to see. Absolutely. Good. I know we're actually already a couple of minutes over. So maybe just as we're wrapping up here in summary, we touched on a lot between a really in-depth discussion in HCC. So we really appreciate you being here again, Dr. Li. And then so yeah, across both Casdozokitug and Tagmokitug. So just kind of as we're wrapping up here, leave investors with why they should be paying attention to Coherus in 2026 and what their expectations should be for the upcoming year. So I think we've talked about the data, right? So I think we have a very promising pipeline, first-in-class agent, potentially best-in-class agent with Tagmokitug as well. Basis is the foundation is that we've shown some very nice data that we've talked about already. And I think 2026 is really going to be a data-rich year. And we are very, very excited about what we can really offer patients in terms of the potential for real benefit. Great. Well, thank you so much, Theresa and Rosh and Dr. Li for being with us, and I'll hand it over to Mike just to wrap up. Yeah, thanks, Colleen. And I'd like to echo that. Thanks from my end to both Theresa and Rosh and Dr. Li. And then for the investors on the line, thank you so much for joining us. If you'd like to connect with Coherus Oncology through the balance of the year or early next year, we'd be happy to connect you. So just please reach out to your Baird sales rep, Colleen, or myself. But I hope everybody on the line has a happy holidays. And thanks again to all for joining. Thank you. Happy holidays. Bye-bye.