All right. Good morning, everyone. I'm Stephen Willey, one of the senior biotech analysts here at Stifel. Glad to have with us, as part of the next session, the CEO of Compugen, Eran Ophir. Eran, thanks for joining us today. Thanks, Steve. Any opening comments or introductory statements you wanna give before we jump into Q&A? Sure. Maybe consult a few words, high level description of Compugen. Compugen is a pioneer in AI-based computational discovery. We're doing actually AI before all of this recent hype of AI, and we use this AI-based platform to identify new drug targets in the field of immuno-oncology. We have a validated computational platform, and why it's validated, because we showed again and again we can use computational tools to identify new drug targets. We have internal assets that we'll describe together in the discussion today that were discovered using our computational platform. The platform is validated by the collaboration we do with pharma companies around some of our discoveries, and we'll discuss it as well with Gilead, AstraZeneca. We have, we say the one critical milestone for with the internal asset in the Q1 2027 for COM701, a blocker of PVRIG, unique checkpoint that we identified, very different biology, a very interesting signal in ovarian cancer with the readout of small randomized study in Q1 2027. We have a collaboration again, we'll discuss it around the bispecific antibody rilvegostomig with AstraZeneca, which is in 11 phase III trials. Another collaboration with Gilead, another asset, GS-0321, a cool approach to harness cytokine biology for the treatment of cancer. Behind all of that, we have a whole pipeline with innovative approaches to activate the immune system against cancer. All of that is derived from this computational engine that we use to identify drug targets. All right. Very good. Maybe we can start with the adaptive platform trial that's evaluating single agent COM701. Again, this is the anti-PVRIG antibody. You're looking at this as maintenance therapy in kind of second-line plus platinum- sensitive ovarian cancer patients. Can you just remind us kind of what the framework of the trial looks like here with respect to patient numbers, randomization, endpoints, and then maybe just any kind of specific baseline characteristics that you're targeting for the purposes of patient enrollment here? Sure. Maybe we can start by two sentences what brought us to this study. PVRIG, as I mentioned before, is a unique checkpoint with a very different biology. They're very different from PD-1, definitely from TIGIT. From the beginning, ovarian cancer was an indication, target indication for us because of the biology of specific biology of PVRIG. In general, the pathway is very dominantly expressed in ovarian cancer. We started the clinical trials typically done last line patient, platinum-resistant ovarian cancer patients. We saw and we presented in ESMO last year a pooled analysis of COM701 in monotherapy and combinations, and the signal was quite clear. We saw activity of COM701 in these last line patients and in monotherapy and combinations. The patient who did get clinical benefit, it was very durable. The safety profile is excellent. We decided with discussion with KOLs, that for this type of drug, with the safety and durability and mechanism of action, we should actually go earlier in the ovarian cancer treatment algorithm. What we identified together with the KOL, that in the second, third- line, platinum-sensitive ovarian cancer patients, so these are patients which still respond to the platinum. They are much earlier than the we treated patients. Some of them were after 10 prior lines. They are much earlier in the treatment algorithm. They have less exhausted immune system. We take only patients which are platinum sensitive and responded to the last platinum-based chemotherapy. They'll have low tumor burden, and we exclude patient with liver metastasis because we discovered that these patients are doing much better in response to COM701. We're increasing the probability of these patients to respond to COM701 by selecting this specific earlier line patients. There is a huge unmet need for these patients because in the second, third- line, platinum-sensitive ovarian cancer, patients who already received bev or PARP are not eligible for bev or PARP, there is no standard of care. There is a huge unmet need. This patient received the platinum, they respond to it, but soon enough they will relapse and eventually become platinum- resistant. To find a drug that prolong the response to the platinum is a huge unmet need, and this is the MAIA ovarian trial. We're taking second, third- line patients, platinum- sensitive, responding to chemotherapy without liver metastasis. We are randomizing them in a blinded randomized study. Forty patients will receive COM701 monotherapy, 20 will receive placebo. Nothing, because again, no standard of care, so we can do that. The readout is gonna be a progression-free survival with the readout in Q1 2027. This is the MAIA trial. You're excluding patients who have baseline liver mets. This is not uncommon for other IO-based studies that we've seen in other tumor types like colorectal. What proportion of the patients? [crosstalk] colorectal, yes. What proportion of patients would you expect to screen out on the basis of having liver mets at baseline? We don't have the exact numbers, but overall, our estimations also with discussions we have, that in these relatively early aligned patients, probably not much more than 10%. It's not going to be huge patients excluded, but again, we think that it allow us to further focus on patients that are more likely to respond to COM701. In the PROC settings, in which also the higher frequency of patients with liver mets, we had like 4 x more clinical benefit in patient without liver metastasis compared those with liver metastasis. That's why we're doing this exclusion, even though we go earlier. Okay. Maybe you can talk about your assumptions for progression-free survival in both the placebo and the COM701 arms, and maybe specifically speak to your level of confidence around the placebo arm assumption and, you know, maybe how that assumption is sensitive to the type of clinical benefit that a patient achieves with platinum therapy. We're focusing only on the patient which respond to the platinum, so either complete or partial response. Based on the older trials, mostly the PARP trials that were done in these settings in second, third-line ovarian cancer, a patient who respond to the platinum and then receive maintenance. The range, it is between 3.8 to 5.8 months after finishing the platinum before the patient relapse. This is the median expected PFS. This is our expectation that will be somewhere in between this range, 3.8 to 5.8 months. Okay. Quite stable across studies. Yeah. Yeah. I know that you've, you're guiding to interim data here from this first analysis occurring in the first quarter of next year. Will this be a analysis that determines either a no-go decision? Is there a futility assessment associated with this as well? Absolutely. Our goal here is to see a clear-cut monotherapy signal for COM701. There is a futility analysis. In general, we want to see this decision point for us in general, if the signal is positive, not borderline, clearly positive, seeing monotherapy signal, then the first thing that probably we should do because of dynamic need is start discussing with the FDA about the registrational strategy. This will be the first thing. Then because this is an adaptive trial design, we can also now after proving COM701 is active in ovarian cancer in monotherapy, we can also build the whole strategy around, for example, we can test now one arm, easily an arm, combination with ADCs that are emerging agents in this field. We can add an arm with PARP and then consider going into first-line maintenance. We can also think in general going into last line patients again now with pembro and docetaxel, which was recently approved. After proving and not to talk about other indications, which we have seen signal, I think after clearly showing COM701 monotherapy signal, first we go for registrational strategy in this patient population, but then the expansion could be quite broad in ovarian and outside of ovarian cancer. Okay. Presumably the safety data you've seen would give you a lot of flexibility on kinda what you choose to partner with... Absolutely. in terms of... Absolutely. in terms of combination therapies. I think it's both in terms of safety, also in terms of the mode of action. For example, ADCs, the mode of action is extremely complementary with the mechanism of action of COM701. Same goes for other potential agents. Yes, combination. After proving the efficacy, the combinability of this agent should be quite strong. Is the thought process around the potential synergy with an ADC, is that driven by this notion that, you know, these agents are highly cytotoxic, and as a result of their activity, you almost kinda get this MSI-H, TMB high type of signature that then primes a patient's ability to respond to something like COM701? Yeah, I'm not sure it's exactly gonna transform a cold tumor to become like MSI-H, but it definitely will induce some signals and antigens, and specifically the biology of PVRIG. We'll not go today into all the details, but dendritic cell biology, antigen presentation, stem-like memory T cell interacting with disease. This specific biology can work very nicely with the signals generated by ADCs and cytotoxics in general, but yes. Okay. Maybe the last COM701 question, and then we'll get to the earlier stage pipeline. How are you guys thinking about the addressable market opportunity here that exists in kind of this second-line plus maintenance setting for COM701? I know that there's a decent amount of epidemiological data for second- line, but then I think as you get beyond second- line platinum- sensitive, that data's a little bit less clear. What's kind of your best guess as to what the TAM looks like here from a patient numbers perspective? Yeah. For that specific population, a patient who received bev or PARP or are not eligible for bev and PARP, these are typically second or third- line platinum-sensitive patients, our estimation is roughly around 8,000-12,000 yearly. But then again, by adding more arms, for example, if we just add bev to this combination, this is another combination we can do, we're already getting most of the second or third- line, the numbers increase to think around 30,000. The initial patient population probably around 10,000, we can easily go broader, as I mentioned before. Okay. You also have the GS-0321 partnership with Gilead. This asset's currently in phase I dose escalation in solid tumors. Can you just speak to the progress that's been made on this program thus far? You know, how engaged are you with Gilead around the progression of this program and what next development steps might look like? Mm-hmm. Really in short about the program itself, so I think this is another program that we identified computationally. It's not only a first-in-class asset, it's a first-in-class approach in which we harness cytokine biology for the treatment of cancer, with a very differentiated approach using an antibody and not an engineered cytokine. We think, and showed preclinically, that this approach can overcome many of the challenges that others had and are having in these attempts to engineer cytokines to use them as the anticancer agents. This is a really cool approach and a different one, and it's very exciting to take this kind of approach to the clinic, and it's even more exciting to do it with a great team like Gilead. There is very tight interaction. The teams are working together. We are leading the phase I trial, even though the asset was licensed to Gilead. We're leading it, but it's tight interaction and a very good collaboration for this trial. In general, the way this trial is built, it's solid tumors, all comers, dose escalation in mono or in combination with zim, the PD-1 of Gilead. In the dose escalation, we also have a few backfill cohorts in different doses. We have the second part of the phase I study is the dose expansion in selected indications, which is also run by us. By the terms of the collaboration, after we end the phase I, Gilead will take it to phase II and further on. Because of that collaboration, obviously, we cannot disclose specific details on where we're standing, but we did start more than a year ago. We dosed the first patient at the beginning of 2025, and the trial is progressing really nicely. Hopefully, with discussion with Gilead, we'll report results a bit later when the trial progress a bit more. Maybe to that last point, will you be able to present some of the dose escalation data before you move into dose escalation? I know sometimes these larger partners, you know, aren't really incentivized to give you bite-sized pieces of data that often benefit a smaller company like yourself. It's a good question. I mean, we have very good collaboration. Gilead are aware of the fact that they're working with a biotech that have this need to disclose data, and we are also sensitive to their needs. Looking at other collaborations they did, I think that they did allow in some cases to release also early data. We cannot commit for now, but definitely in discussion with them, I'm optimistic that we're able to release data sooner than later. Again, we cannot commit. Okay. Maybe you can just kind of talk to the longer term economic leverage that you have to the success of this asset, and if there's anything that you can say about the potential cadence of milestone payments and whether there's meaningful milestones that could be earned within kind of these early stages of development. For this deal, we received to date $90 million. We received $60 million upfront and $30 million after achieving the IND clearance. We're eligible for additional $758 million and up to a low double-digit tiered royalties. About how the milestones are splitted, we cannot say much. What I can say that typically these kind of collaborations, when you move from stage to stage, there are milestones. As I mentioned before, the phase I is splitted into the phase I-A, dose expansion, and phase I-B, dose escalation and then dose expansion, and then phase II. We cannot give much more details on exactly where and how much we'll get the milestones. The other partnership that you have, which is probably generating a lot more investor attention right now just because it's been made a lot more visible, is rilvegostomig with Astra. This is a TIGIT PD-1 bispecific. Astra now has this in 11 phase III studies. They've attached $5+ billion of peak sales guidance to this. I know TIGIT has been a pretty disappointing target, which might be the understatement of the year. We recently saw Arcus and Gilead discontinue the dom program. You know, what gives you and Astra, you know, the confidence that rilve can change the narrative around this target, around TIGIT? This is a very important question. Now I'm not speaking on behalf of Astra, so I will say what I think, being the one company discover TIGIT and studying TIGIT for so long. There are three aspects for that. It's the format of the antibody they use, the bispecific antibody, the combination strategy, and clinical strategy, and I will explain. First of all, most of the failures of the TIGIT were with the Fc-active TIGIT antibody, terrible safety, difficult to combine. Let's park this for a second because Arcus also failed with Fc-reduced. The Fc-reduced gives you the option to combine very easily, and still I think it should be more efficacious than Fc-actives. Also comes the bispecific portion. AstraZeneca have shown preclinically. In a very translational system of material taking directly from patients, ex vivo system, they have shown that the bispecific, probably due to its cooperative binding, is different than just PD-1 TIGIT combination, and actually it's more efficacious than PD-1 and TIGIT combination tested thus far. One, the bispecific by itself could be, should be more efficacious, at least based on this data, and the clinical data will have to prove it. This is one. Two, which is also in part because of the bispecific, the combination strategy. When you have a bispecific that blocks PD-1 and TIGIT, first of all, the burden of proof for contribution of components could be easier in some of the trials. Again, going back to the Fc- reduced, this allow you to combine, and you look at the strategy of AstraZeneca across the 11 phase III trials, they are really combining many ADC combination with ENHERTU TROP2 ADCs. In some of the studies, the way I see it, they don't really have to prove that TIGIT is active as part of the bispecific to get the win in that specific trial. For example, there was a phase III trial of rilve plus chemo versus chemo. They use it as an IO backbone, as a KEYTRUDA-like molecule, if you may, and this trial is not testing TIGIT activity at all. It just rely on the fact it's a safe, in the worst case, very good PD-1. I think that it does target TIGIT, and it is more active than just PD-1. Other trial they are doing, for example, rilve, TROPION-Lung10, rilve plus TROP2 ADC versus pembro in the TROP2- selected biomarker patients. I think there is good probability of success regardless of TIGIT being active or not. Again, I think that we know that TIGIT is active. The question is it active enough to gain a phase III success? This is the combination strategy. Lastly is the trial design. I think the way I see the way AstraZeneca designed their trials, that they learn from the mistakes of others. They are powering the studies in the right way to fit for the magnitude of effect that TIGIT can give. They are focusing more, for example, Arcus in their recent failure in the non-small cell study. At least they started as all-comer study. They did adjust along the way to focus on PD-L1 positive. I'm not sure about the numbers. AstraZeneca are selecting PD-L1 to begin with. They are looking at squamous versus non-squamous separately, each study nicely powered. I think also this clinical strategy is learning from the mistakes of others and potentially fits more the biology and the magnitude of effect you can expect from TIGIT. It was kind of a long answer, but I think it's covered nicely the three aspects, the format of the antibody, combination strategy, and clinical strategy that along the 11 phase III trials should allow at least to some of them, if not most of them, to be successful as way I see it. Yeah, no, it's a good point, right? 'Cause I guess where the TIGIT translation has failed has been in that, you know, phase II to phase III transition where you then need to show superiority versus PD-1 alone, and that's kind of where a lot of these assets have fallen short. The way Astra has designed these studies, you don't necessarily need to show superiority relative to pembro, and you can lean on some of the other agents that they're including in the combinations to get you that win. I think we're gonna be getting some updated data from Astra at the upcoming ASCO meeting. Anything that you think is worth highlighting to investors in terms of having important read-through to what they're doing in phase III? There is one study, the I-SPY, combination with ENHERTU, and this is in breast cancer, which they don't have any phase III study ongoing. I think that there are some other interesting studies, phase III studies of rilve in combination with this amazing blockbuster drug ENHERTU. I think still signs of efficacy versus historical data and the safety and combinability are gonna be important and some read-through to the ENHERTU combination studies that rilve is doing in phase III. There is hepatobiliary study, non-randomized study, 30 patients, I believe. Still, there is an ongoing equivalent phase III study, it will be interesting to see rilve plus chemotherapy. We don't know if there will be OS data or just PFS data, it will be interesting to see some comparison in terms of safety and efficacy compared to historical, mainly the durva control in the TOPAZ-1 study, which is the control arm in the phase III study. I know you recently monetized a portion of the royalties that are owed to you from Astra, with Astra. Can you maybe just talk about the rationale for that transaction? Why was that the right time to do it? How does the structure of that transaction preserve your longer-term leverage to the success of this drug? Yeah. This was we did it at the end of 2025, and the rationale was that we monetize a very small portion of the royalties we had. We had mid-single digit tiered royalties before the monetization, and we remained eligible for mid-single digit royalties after. We really monetize small portion, meaning that if rilve will be the blockbuster we believe it in, we still have full potential to receive these mid-single digit royalties. For this amount, we receive $65 million upfront. Additional $25 million for the next milestones. Totally we're eligible for additional $195 million. We're receiving this cash now, we have the cash runway into 2029, and this will allow us to achieve internal and external milestones and to be there to receive potentially the next BLA acceptance milestone from AstraZeneca. I think this was a great combination of giving us the runway to continue and invest in our pipeline. The early pipeline we didn't discuss, but we have the computational engine, and we'll continue to invest in the early pipeline. This cash runway was exactly on time to allow us to continue execute aggressively on all fronts and to be there eventually to enjoy potentially from rilvegostomig clinical success in phase III. Okay. Maybe just last question, you know, the earlier stage discovery efforts, the computational platform, how big of an effort do you have ongoing here in the background? You know, how do you think about the balance between capitalizing on BD opportunities like you pursued with Gilead versus, you know, building out a wholly owned pipeline that you guys can lay claim to? We invest huge efforts in the early pipeline. We have this engine, it's a validated one. We believe that the assets coming from this agent can really make difference to patients. The largest team in Compugen is actually the one who works to continue bring such assets. About how we see keeping it internally or out-licensing, I think that now when we have the financial stability, we have the freedom to decide. In the past, and as many typical to biotechs, you have an asset, you're running out of cash, you have to out-license it. The Gilead deal was an amazing one, $90 million, et cetera. Now we have the freedom to decide. We may want to keep the asset to ourselves if we think that we can generate more value to investors by keeping the asset, maybe generate a phase I data or more. We also have the flexibility to decide, okay, for this asset, if we think that the right thing for this asset is to go early on to pharma companies and to move it aggressively in the clinical pipeline, we can make the decision. I think now with the financial stability, we also have more flexibility to make decisions and potentially to maintain more value and keeping more assets and not necessarily licensing out early. All right. That's all we have for time. Eran, appreciate it as always. Thanks. I'm sure our paths will cross in Chicago here in the next week or two, so. Absolutely. See you there. Thanks, everyone.