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Good afternoon, everybody. Thanks for joining us here for the next session. Really pleased to have Coheris 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, Coheres 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 First of all, of course, we have a next-generation PD-1 Torpalmab brand named Lactorsi, which we launched into MPC, which is moving along quite well. This has demonstrated differential activity against Gatruda in a number of settings, and I think primarily the MPC 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 Treg 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. and 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 can you just sort of, for everybody's benefit, talk about how big you think that product can be and obviously sort of from a business standpoint what that provides for you as you're developing the pipeline? Sure. 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, if 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, the company, which, of course, is our focus. We project that next quarter, probably in the second half, Q3 or 4, that we'll 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 Humira biosimiler, 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 will be able to, I think, hit a plateau on a quarterly basis. So, you know, that's like 40-plus per quarter, and 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 time frame, 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 a six- year survival data of the NCCN 1A guidelines and so on. And it's an education 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, buying enough data to where we understand where 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-2. 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 Tegmo-Ketog, the anti-CCR8, 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 it's a differentiated story. I think 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, you know, 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 they were open to collaborations and working with others and so on. But that certainly is top of mind. Okay, great, great. So CCR8, Tregs, look, I think investors have heard a lot about Treg. I 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 to do that. Do you have a right approach here? Sure. 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. Treg 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, you knew, Treg Depletion frees the immune system, 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 I had the next study, the 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 toropalimab, so the activation of T-cells pursuant to PD-1 administration. But that was very, very exciting. Based on that data, Raj 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 CCR8 agents. This was, you know, the discovery that the T-regulatory cells in the tumor microenvironment were differentially expressing CCR8 on their surface was made, you know, by Rudinsky and company in 2016, Morosal and Kettering. And the race was then on to try to find molecules that would attach to that CCRA 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 has been very difficult to find sufficiently selective agents to do that because if you make an antibody, it'll cross-react with a lot of other 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 CCR8, which is quite good. So we believe we have a best-in-class asset. but 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, Rosh 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 CCRA 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-linehead 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, Rasha, do you want to talk a little bit about the second-line head and neck study? Yeah, absolutely. Thanks, Denny. 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 next squamous cell program. Protocol two is the GI program that essentially Danny mentioned, which has four cohorts. It's second-line upper GI adeno. It's first-line and 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 pathoridomig. 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 askings. For the first-line esophgeal squamous cell cohort, we are 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 early in the colarectal space. And, of course, pasoridomig, we are asking the novel, novel question. So what we've communicated so far in the second line head and neck study, the 40 patients, it's totally 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 involving head and neck space as well. Secondly, we communicated that we are seen activity both in terms of response, but also in term of duration. That duration is very imporant 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 CCRA 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, etc., in particular the EJFR bispexifics, 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 to that. So we'll also likely get PDO data before the end of the year, it sounds like. So that's obviously a different piece of the map. the, so, you know, how does that, 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 pedo yes absolutely but that's what I was alluding to in terms of the EGFR by specifics pedo in particular so pedo 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, et cetera, et zebra. 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 for 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 Tegmon-Ketog appears to be working much better in HPV positive, and And there appears also to be an opportunity to select patients on the basis of CCR8. 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 CCRA is so could you just talk a little bit about the plan from here so you'll get some of this data in 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 difficult to answer in the absence of data. But I'll answer the hypothetical regardless. I think, first of all, as Rush 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 interoperability 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 RPD1 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&J with T-cell engagers, right? A T-cel engager needs a T-celle to engage. And if there's not one in the tumor microenvironment because they've been excluded by Tregs, 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 Rosh is investigating to see how the presence of CCR8 and, you know, the signal are correlated. And I think that would be very interesting. So if we see consistency, for example, you know, from CRC and esophageal and gastric and so on, you know, and even head and neck, and we understand how we can follow this signal, 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 two program and see what's very promising where we can roll into a pivotal. Okay, great, great. So maybe we should switch to IL-27. I think as you referenced, right, the biology there is known. I guess the question is, how did you pick the tumor types that you think, you know, 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, then I'll, you now, let Raj talk about the basket study that we did. So IL-27 is quite interesting. It's actually one of my favorites because of the 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, LIG-3, and all these different things. Secondarily, it downregulates the expression of all the inflammatory cytokines, interferon gamma, and so on. And thirdly, 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 was quite interesting. I mean, what we did is we did a basket study across a number of cancers. And, Rasha, why don't you just update on how that came out and how we got to the indication selection? Yeah, so as Denny said, so 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 tumortypes, some as monotherapy, some als combination. So following that, we did move into first-line HCC. Obviously, there's potential to move outside that, but our initial area for exploration based on that initial study is first- line HCCC. 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% CR rate. 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 Atizubev alone has given is 30%. And also, I mentioned a 17% CR rate. What Atizebev alone have 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 Atizobev 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, right? There was no added toxicity over and above the toxicities of atezobev alone. 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 for sign HCC. We have the potential to expand into additional tumor types as well. Yeah. What I like about the Casdozo program is we're on the follow-on study already, right? Whereas with the Tegmel program, you know, all well and good, but really they're single-arm studies. They're not controlled. Casdozo has two doses of Casdoza, high and low, together with toropalimab and bev, versus toropalamab and beb alone, right? So you'll be able to see the IL-27 response. You'll be to see if there's a dose response, and you'll 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, you know, a lot of adverse events. It's very much just like using a TezoBev 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 if I 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, Casdozo 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, you know, 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 to 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 Atizo for Tori two doses of Casdozo in combination with ToriBev versus ToriBev 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 allow us to to get data towards contribution of components with the Tori Bev arm alone to see what CasDoZo adds on top. That's what the study is, that's what the aim is. So we completed accrual to the study around March. We are now just waiting for that date to mature. What we anticipate is that the initial effect will be due to VEGF. So that'll be the VEJF 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. I'm sorry, I was just going to follow up on Rasha's remarks because you asked about the potential pitfalls. The other attractive thing with Caszozo 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 in Tegmo and Keetig where if you look into a second line or a first line indication and somehow you can go, you know, on top of standard of care, I think that's a better bet and a good spot to be in. Yeah. Yeah, 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 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 a call 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 early in the response. With PD-2 treatment, you see it on the tail, just like with toropalimab, 67 months of response, 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 that's how 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 this study is biomarkers, of course. So we're going to be looking at baseline IL-27 levels, but also ctDNA as well. And that could be actually an early indicator of activity as well as level of baseline disease. Perfect, perfect. um maybe just to to round us out obviously your biotech company cash is an important component of the business here so how are you thinking about your runway how areyou thinking about you know well the one well you know the one thing about being a public biotec company is people have very good visibility into your cash and your burn most at most times um i think we do a really good job with our cash and managing our cash uh and going forward i i think were very good uh 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, 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 breakeven 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 this study they come they can vote with their wallets and i think that's really what you have to do you have and the investors that we have talked to though when they look at our studies particularly you know like the casdosa study where it's controlled and so on you know i think they view that favorably and the feedback that we've gotten from investors on how we're proceeding with Tagmo Ketug and understanding the biology of Treg depletion is very, very positive. You know, we're not out there just, you know, throwing mud on the wall trying to understand what's going on. We're very systematically working through a number of cancers, a number lines of therapy. We are 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. Thank you.