Good afternoon, and thanks for joining us to have a conversation with Eran Ophir, President and CEO of Compugen. Compugen is a clinical-stage cancer immunotherapy company, and a pioneer in computational drug-target discovery, powered by AI and ML. Its Unigen platform has already discovered the targets behind all three of the company's clinical assets, the wholly owned LEAD program, COMP-701, a potential first-in-class anti-PVRIG antibody is in MAIA, Ovarian, study randomized placebo-controlled adaptive study which is testing the drug as a maintenance monotherapy in second and third line relapse platinum sensitive ovarian cancer and we are expecting some interim data especially in the first quarter of 2027. So the company's partner AstraZeneca is advancing Relvagostomic the PD-1 digit bispecific, you know, whose digit component actually comes from Compugen's 902 program. And that's the partner is actually testing it out in 12 ongoing phase three trials and the third one is the Gilead is advancing the anti-IL anti-IL-18 antibody which is GS0321 currently in phase one. So to talk about all these programs and how the pipeline is progressing, I invite Iran to this Fireside Chat. Thank you, Akri. Great to be here. So Iran, you know, for folks who are really new to Compugen, you know, what's you know, what's the platform, what's the Unigen platform itself, and how has that helped generate these targets that you're testing out against? So Unigen is a platform that we built along years, and first what is unique about, because we are focused on the very first stage of the R&D process, the targets themselves. Many people are trying to use AI to generate in silico antibodies and optimize, but we are focusing on the first stage to really bring new mechanisms, very challenging task, to really bring first-in-class assets but we believe this is where we can make most of the impact for patients and bring most of the value for our shareholders. And we're using this by building this database we built along years with mapping the tumor environment from every different angle, proteomics, single cell, special, and then we have this database which really characterize the tumor environment to every different angle and then we use our algorithms and know-how how to derive targets and eventually take this first-in-class assets into partnerships, into the clinic eventually, and I think this is another thing which is unique about the platform, it's not just another AI hype company, we're doing it for years and the platform is validated by our clinical assets and by our partnership with Gilead and AstraZeneca. So talking about the partners, you know, Gilead and AstraZeneca, and plus your own clinical candidate, where do you think investors are giving you value and where in which of these partnerships are your program is investors not really paying attention at this point? So I think these are the main three pillars, I think the point which is maybe missed a bit and it's obvious because we didn't give enough data yet but it's the early pipeline and we have this engine that generated all these assets and we obviously work very hard to bring more such assets and but eventually the proof will be in the pudding in us being able to bring more. The COMP-701 study was the result in Q1 27, I think it's a very important readout, we'll talk about it a bit later about how about the animate need and the options over there. And you know, Relvagostamig is in 12 phase three studies. Yes, it's a digit molecule, I understand it disappointment that investors had from digit, but if people really look into the details and see how Relvagostamig is different, it's the only bispecific digit PD-1 antibody that is tested, the way the clinical strategy is being built I think that there's for sure something which is being missed by investors over there in the value to give to Relvagostamig. Yeah, I think this is the main points. So regarding COMP-701 and the MAIA ovarian study, you know, can you highlight what the study is set up to do and in terms of the patient patients that you're targeting, you know, what do they currently have in terms of therapy and how do you see COMP-701, you know, managing that population? Sure. So let's talk for a second about the treatment algorithm of metastatic ovarian cancer patients. Typically they're diagnosed late, they either receive surgery, and they receive platinum chemotherapy. Platinum chemotherapy is extremely toxic, they can tolerate four to six cycles max, and then they need something to maintain the response if they responded. In the first line there are options like PARP or BEV, but when they reach the second, third line, and if they are still platinum sensitive that they responded to the platinum, four, six cycles, they cannot tolerate more, it's too toxic, there is actually no standard of care to maintain these patients and to prolong the time they are still platinum sensitive responding to the platinum before they're becoming platinum resistant. So the trial that we are doing, the MAIA study, is focusing on exactly on this huge animate need, second, third line, platinum sensitive ovarian cancer patients, the respond to the platinum and then the randomized to receive 40 patients receive COMP-701 in monotherapy and 20 are getting placebo and there is a randomized blinded study with the goal of really see can COMP-701 prolong the time the patients are off platinum and without relapse. So during the second quarter call, you announced the lowering of the assumed placebo median PFS to roughly four months you know from about five and a half months after looking at the data from Tedova and Oreo. Which showed 2.8 month control arms in more heavily pre-treated patients since your currently blinded and it is a randomized against an internal placebo. You know, how much should investors weigh that external benchmark if at all? So, you know, eventually it is indeed a randomized blinded study and that's why we have an internal control. And this is for sure the most important, the comparison of the patients receiving COMP-701 to placebo in that study. However, this is not a phase three study, it's not powered to be a phase three study and therefore especially in this context to have the historical benchmark, the historical context by the way even to the Bayesian statistics, the historical control contributes. So for this kind of studies, while the main comparison is to the placebo, also having the context and the historical context is important and that's why we aligned expectations of roughly where it should be the PFS of the placebo. Okay. So talking about PFS of the placebo, you know, you said you think six months after platinum-based chemotherapy is clinically meaningful. You know, what's the rationale behind that and you know, do you think that's the right threshold? So by definition, if patient is responding to the platinum, and if they maintain the response for more than six months, by definition they are classified as platinum sensitive. Meaning that if the tumor eventually relapse after seven, eight, nine months, they're going to receive platinum again. If they are not responding to the platinum, or if the patient are relapsing before six months, they are being categorized as platinum resistant, they are moving to different type of therapies, they have worse prognosis, so by definition, from clinical perspective, if you can maintain more patients platinum sensitive more patients with this chemo chemotherapy free break for more than six months, this is going to be clinically meaningful, eventually to know if we are if we have a strong monotherapy activity that is enough for us to go into phase three, it will be not only six versus four months, it will be also looking at the totality of the data, separation of the curves, all the readouts and to see are we really convinced that this signal is potent enough to drive a phase three success, which is eventually obviously our goal. Okay. So in terms of timing, you know, you said the interim analysis would be the first quarter of 2027. Even with the shorter you know placebo assumption that you currently have. So is that because it's more an event-driven event event-driven trigger or is it a follow-up time? No, eventually the change in the assumption for the placebo from 5.5 to 4 didn't change much in our assumption for the trial. I can just say that overall we believe we are fully on track to report the results of the median PFS, which are eventually the meaningful readout from this study by Q1 27. Okay. So do you see this current trial as registrational and if it's not registrational, you know, what data are you seeking from this study so that you can actually plan for a registrational study? So indeed this trial is a 60 patient study, it's not a registrational study, it's not powered for example for statistical significance. It is being following the Project FORGE, one of the FDA, it is being designed with the Bayesian statistics, eventually our goal is to see a convincing COMP-701 monotherapy, we have 40 patients receive only COMP-701, whatever anti-tumor activity we're going to see is going to be driven by COMP-701 compared to the randomized placebo control. Eventually we need to see a totality of the data, separation of the curves, the PFS value obviously, and to see are we see a convincing COMP-701 activity. And the magnitude of effect is also important for us to be able to design the phase three study. So this study by itself follows Project FORGE, theoretically could lead to accelerated approval. Anyway, even for accelerated approval, one needs to have a phase three design and the goal is to have this study to guide us on the phase three design. Okay. In terms of the study, in COMP-701 activity, you know, you expect that to be seen in both PD-L1 positive and negative patients, but at the same time you have excluded liver met patients, right? So beyond the PFS, you know, are you looking for additional biomarkers so that you can try and increase or broaden the population itself? So first of all, I think it's very important point to discuss the data we have seen. So when you treated the last line patients, platinum resistant, this is where we started, typically this is where you start drug design. In the last line patients, we saw responses for COMP-701 in monotherapy and combinations indeed in PD-L1 positive and negative. And why is that important? Because checkpoints like PD-L1 and TIGIT for example, even when combined together, historically gave zero percent response rates in PD-L1 negative over end cancer. This doesn't mean that we had activity only in PD-L1 negative, it doesn't mean we're going to enrich for PD-L1 negative in our trial, it does exemplify the unique biology of PVRG and that we saw these signals in last line patients. Which are probably driven by COMP-701 compared to historical control. Then going into this study, what we did is trying to enrich not by a specific biomarker. We tried to enrich by selecting the patients which are most probably to respond to COMP-701. A bit similar to the Moderna concept that they started in metastatic melanoma and then went earlier with their vaccine, we started late in last line patients, we're moving earlier in the treatment algorithm into platinum sensitive ovarian cancer patients. We take only patient to respond, low tumor burden, less compromised immune system, we're excluding indeed patient with liver metastases because we saw in the last line patient that by that we are enriching for responders. So overall we're trying to enrich by selecting the patients which are most probably immunologically to respond to COMP-701 and the readout is going to be mostly median PFS, this is the definitely the important readout, but any other measurement of anti-tumor activity we could measure will obviously look at it and see indicating for COMP-701 monotherapy activity. And so moving on to the AstraZeneca's work on Relvecoz topic. Right? At ASCO, 2026, they presented, you know, the first overall survival data which was 16.8 months median OS in the first line biliary tract cancer against historical trials which showed less than 13 months. So given some of those disappointments that we have talked about previously with the TIGIT, you know, how does what's the contribution of that particular readout and, you know, you know, how do you think that plays against PD-L1 of the biospecific? So eventually obviously we need to see a phase three success period for Gustamig. Meanwhile we see again and again in this single arm non-randomized studies, compared to historical controls, how Revogustamig is indeed an actually the way AstraZeneca's management describe it in the recent ASCO call, stabilizing the responses. Seeing starting to start to see more and more PFS and OS readouts which are the important readouts eventually for phase three success, just this morning they reported another very interesting results in non-small cell line cancer. Again, it's a non-randomized study and still PFS, OS readouts very promising in some of the readouts more than doubling compared to the historical control. So this is looks very promising. But yes, eventually especially for TIGIT, especially after all the disappointment, we will need to see some of these 12 phase three studies being successful. What is interesting about the molecule of AstraZeneca that because it's a biospecific, PD-L1 TIGIT biospecific antibody, nobody can ask them to take out the TIGIT arm and to show directly contribution of components. So to show that TIGIT is working in their hands, some of the studies are doing direct comparison of Revogustamig to PD-L1 or PD-L1 blocker, this is one type of studies. But actually some of the studies don't even ask the question is TIGIT contributing. For example, when they have a study using Revogustamig is a IO backbone. This is the IO backbone of a combination. And they're combining it with an ADC. And compared to standard of care which is PD-L1 plus Herceptin or PD-L1 plus chemo, they're asking is the combination working better and safer compared to standard of care. But because it's a biospecific, they ask this regulatory benefit they don't have to show contribution of components because they cannot take the TIGIT component out. So some of the studies ask directly is the Revogustamig better than Keytruda or other PD-L1s, PD-L1s. But some of the studies are asking is the combination is working better than standard of care. And Revogustamig is very safe, easy to combine. So the safety is very similar to Keytruda. And the combinability allows it to be used as a IO backbone for next generation combination, mostly ADC combinations. Okay. So AstraZeneca is publicly said, you know, that they see this as a $5 billion opportunity. And then you have an agreement with them which is about $195 million still remaining in milestones. On top of the mid single digit royalties. So you know, what is it's it'll be helpful if there is a way you can talk through the cadence of how these milestones roll out. Yeah, well unfortunately it's typically to a pharma biotech interactions we are not allowed to say much. But what we can say that we're eligible for $195 million, that the next milestone is BLA acceptance, which is probably somewhere following the phase first phase three success. And then this mid single digit royalties which if we did we talk about more than $5 billion of potential sales are going to be very meaningful for Compugene. So on the Gilead agreement or partnership, you know, what sort of data should we expect next? And you know, and also you know, what do you think should the data show so that we see that moving into the next stage of development? So I will not speak in behalf of Gilead. I would just say there's typically this is a phase one study in mono and combination with Zim the PD-L1. And the goal is really to see safety the dose recommended dose and obviously all of us wants to see as early as possible some signs of anti-tumor activity. We cannot say much here as well about the agreement. But we are eligible for additional $758 million we received already $90 million. Gilead will communicate discuss with us when to disclose data. For sure when moving from stage to stage we're going to the typically milestone in this kind of these and then we're going to report at least the milestone agreement. But I think that eventually we're also probably will discuss the results themselves but for now unfortunately we don't have specific guidance for when. And regarding Comp 701, you know, if it delivers the PFS prolongation that you know, you're expecting to see you know, what's the next indication that you know, you could take this combination into and when you get there, you know, do you plan to do it yourself or you know, you are going to engage with another partner just like what you have done before? So eventually we'll see the data and based on it we'll decide if we do it ourself or with partners. Depends on the size of the study. The first immediate goal is to go for that specific population the unmet need. This is where we'll have the results. Phase three trial that we can do alone or with partners depending on the trial. But we saw signals for Comp 701 also in endometrial, CRC, breast. And definitely if we see strong monotherapy activity the goal will to be to go broader and for that maybe we need to co-develop have a partner so but definitely the potential after proving monotherapy activity is broader than ovarian cancer. You closed the second quarter with $125 million in cash and certainly don't have any debt. So what sort of a runway does that give you? And the second part of the question is like what sort of catalyst do investors need to be on the lookout for say let's say over the next 6 to 12 months? So we use a very very conservative assumptions. We have cash into 29 and this financing all the activities you're doing early pipeline, Maya study, all of