Compugen Ltd. Aktie

Ladies and gentlemen, thank you for joining us today. Welcome to Compugen's Second Quarter 2026 Results Conference Call. [Operator Instructions] An audio webcast of this call is available in the Investors section of Compugen's website at www.cgen.com. As a reminder, today's call is being recorded.

I will now hand the call over to Lindsey Trickett, Head of Investor Relations and Corporate Communications to begin. Lindsey, please go ahead.

Thank you, operator. Good morning, and good afternoon, everyone, and welcome to Compugen's Second Quarter 2026 Financial Results Conference Call.

With us today are Dr. Eran Ophir, President and Chief Executive Officer; and David Silberman, Chief Financial Officer. Dr. Michelle Mahler, Chief Medical Officer, will join us for the Q&A portion of the call.

Before we begin, I'd like to remind you that during this call, the company may make projections or forward-looking statements regarding future events, business outlook, development efforts and their potential outcome. The company's discovery platform, anticipated progress and plans, results and timelines for our programs, including disclosure of clinical data, financial and accounting-related matters as well as statements regarding our cash position and cash runway.

We wish to caution you that such statements reflect only the company's current beliefs, expectations and assumptions and that actual results, performance or achievements of the company may differ materially. These statements are subject to known and unknown risks and uncertainties, and we refer you to our SEC filings for more details on these risks, including the company's most recent annual report on Form 20-F. The company undertakes no obligation to update projections and forward-looking statements in the future.

With that, I'll now turn the call over to Eran.

Thank you, Lindsey, and good morning, everyone. Q2 was a quarter of steady advancement, and I'm pleased with the progress we have made across every part of the company. Our science continues to advance in the clinic and our partnerships are advancing on strong footing.

Our MAIA-ovarian trial in platinum-sensitive ovarian cancer is progressing, is on track for the interim analysis by Q1 2027. We're encouraged to see AstraZeneca continue to build momentum behind Rilvegostomig by initiating a new Phase III trial in urothelial carcinoma and with new data at ASCO from the GEMINI study in hepatobiliary cancer and the investigator-initiated I-SPY trial in breast cancer.

Lastly, our collaboration with Gilead on GS-0321 continue to progress as planned. And underpinning all of this is the same disciplined, data-driven approach that has always defined Compugen.

Now, let me take each program one by one, starting with our wholly-owned program COM701, a potential first-in-class anti-PVRIG antibody. We continue to make good progress with MAIA-ovarian, our sponsored, placebo-controlled adaptive platform trial evaluating COM701 as maintenance monotherapy in patients with second and third line relapsed platinum-sensitive ovarian cancer in a setting with no approved maintenance treatment option and significant unmet needs. We anticipate the interim analysis with median progression-free survival data by the first quarter of 2027.

During this quarter, we are pleased to present a trial-in-progress poster on MAIA-ovarian at the ESMO Gynecological Cancers Congress in Copenhagen. The poster underscores the strong biological and clinical rationale for evaluating COM701 in this population, including the differentiated biology of the PVRIG pathway versus other checkpoints like PD-1 and TIGIT, its high expression in ovarian cancer and the durable responses previously observed with COM701 in mono and combination therapy in heavily pretreated platinum-resistant patients.

As we prepare for the MAIA-ovarian interim analysis, we have been keeping close tabs on the emerging external data to keep our own expectations anchored in the current clinical context. Two recent clinical trials in relapsed platinum-sensitive ovarian cancer that included patients who have been pretreated with PARP inhibitors or bevacizumab or both have shown median progression-free survival for the control arm of less than 3 months. While the patient population of these 2 trials is not identical and more heavily pretreated than the MAIA trial population, based on these data, we estimate the median PFS of the placebo control group in our trial to be approximately 4 months.

As a reminder, patients with ovarian cancer are divided into either platinum-sensitive or platinum-resistant categories with the difference being the duration of their platinum-free interval. If a patient relapses in less than 6 months following platinum-based chemotherapy, they move into platinum-resistant category, where further platinum therapy is generally no longer considered effective and treatment shifts to non-platinum options.

For the interim analysis, we define clinically meaningful success as COM701 helping patients remain progression-free for at least 6 months after platinum-based chemotherapy. Achieving these thresholds maintains patients as platinum-sensitive for longer, delays their transition to platinum-resistant disease and give patients a valuable recovery break from the intensity of chemotherapy, thereby improving quality of life, while preserving additional treatment options and potentially changing their disease course.

Overall, we believe COM701's antitumor activity will be best assessed by the totality of the data comparing the treatment effects against our blinded, randomized control arm. MAIA is an exploratory trial designed to evaluate COM701 monotherapy and the magnitude of its effect. It is not a registrational trial powered to demonstrate a statistical difference between the treatment groups. Nevertheless, we believe that comparing COM701 as a monotherapy against a placebo control will allow us to draw clear conclusions about its clinical activity.

Looking ahead, we believe that clear prolongation of PFS in these patients could inform a registration path for COM701 and establish it as a potential backbone for drug combinations in this population, while also enabling a potential broader clinical development plan across earlier and later lines of ovarian cancer treatment as well as in other indications where clinical signals were previously seen for COM701.

Turning to rilvegostomig, the PD-1-TIGIT bispecific antibody being advanced by our partner, AstraZeneca. The TIGIT component of which is derived from our fully-owned COM902 program. In the last week, AZ has added a 12th Phase III trial to the overall rilve program in participants with high-risk muscle-invasive urothelial carcinoma. In this trial, rilvegostomig will be combined with Datroway, their approved TROP2 ADC, and tested in adjuvant settings against standard of care.

This new Phase III trial, TROPION-Urothelial04 follows the Phase II TROPION-PanTumor 03 study in which rilve plus datro combo showed an encouraging efficacy and a manageable safety profile in metastatic urothelial carcinoma.

We're also encouraged by the addition of rilve data AstraZeneca presented at 2026 ASCO Annual Meeting, which we believe continues to support the differentiated profile of this bispecific and its potential as an immuno-oncology backbone across multiple tumor types.

In advanced biliary tract cancer, AstraZeneca presented an updated analysis from the GEMINI-hepatobiliary study of rilve in combination with chemotherapy in the first-line setting. This was the first overall survival data result from rilvi. And as AstraZeneca highlights in their ASCO investor call, the 16.8 months of overall survival was a clear example of prolonged stabilization of responses seen with rilve across clinical trials, and the profile continues to support rilve combination potential.

In comparison, historical trial for first-line BTC showed overall survival duration of less than 13 months. The data showed encouraging efficacy together with manageable safety profile, both of which we view as promising signals in the settings of high unmet needs while recognizing that longer follow-up and randomized data from the ongoing Phase III trial in this setting will ultimately be needed to validate this finding.

As AstraZeneca continues to advance with rilvegostomig across its broad late-stage program, we believe this sustained investment reflects ongoing confidence in rilvegostomig. As a reminder, AZ has previously guided that rilve has a non-risk-adjusted peak year revenue potential of over $5 billion and will remain eligible for future milestones of $195 million and up to mid-single-digit tiered royalties tied to rilvegostomig progress and success.

Moving to GS-0321, formerly known COM503, our potential first-in-class anti-IL-18 binding protein antibody licensed to Gilead. GS-0321 represents a novel antibody approach to harness cytokine biology for the treatment of cancer, potentially overcoming the limitations of direct cytokine administration. The ongoing Phase I dose escalation trial continues to progress as planned. As a reminder, we have received $90 million so far from Gilead on this asset, and we are eligible to receive up to $758 million in additional milestones payment plus single-digit to low-double-digit tiered royalties.

Now, moving to our early pipeline fueled by Unigen, our AI/machine learning powered computational discovery platform, which has been developed and refined for more than a decade to identify novel drug targets and biological pathways grounded in human disease biology. As we have said before, our focus is not on using AI to optimize non-biology, but on uncovering innovative opportunities to activate the immune system against cancer. Unigen has already discovered the targets of COM701, COM902 and GS-0321, and we remain committed to identifying and advancing the next generation of immuno-oncology innovation.

With that, I will turn the call over to David to review the financials.

Thanks, Eran, and thank you all for joining us today. We finished the first half of 2026 with a solid balance sheet and financial flexibility. Cash runway, assuming no further cash inflows, is expected to fund our operating plans into 2029. We anticipate using this runway to continue advancing our COM701 platinum-sensitive ovarian cancer trial, MAIA-ovarian, and to support the progression of GS-0321 in the clinic together with continued investment in our early-stage pipeline.

Going into the details, I will start with our cash balance. As of June 30, 2026, we had approximately $125.3 million in cash, cash equivalents, short-term bank deposits and investment in marketable securities. Revenues for the second quarter of 2026 were approximately $2.6 million compared to approximately $1.3 million of revenue for the comparable period in 2025. The revenues in the second quarters of 2026 and 2025 reflect the recognition of portions of both the upfront payment and the IND milestone payment from the license agreement with Gilead.

Expenses for the second quarter of 2026 were in line with our plans. R&D expenses for the second quarter of 2026 were approximately $6.3 million compared to approximately $5.6 million in the second quarter of 2025. Our G&A expenses were approximately $2.3 million for the second quarter of 2026 compared to $2.2 million for the second quarter of 2025.

For the second quarter of 2026, our net loss was approximately $7 million or $0.07 per basic and diluted share compared to a net loss of approximately $7.3 million or $0.08 per basic and diluted share in the second quarter of 2025.

With that, I will hand over to the operator to open the call for questions.

[Operator Instructions] The first question is from Stephen Willey of Stifel.

I was just curious, so it sounds like you've taken down your control arm assumption in the MAIA trial by maybe about 1.5 months. What do you know about the patient population from these 2 trials that you cited with respect to things like liver metastasis status, and I guess, just general patient eligibility criteria. And I would just be curious to get a better understanding as to your level of confidence now around this revised 4-month number.

Thank you. Michelle, do you want to take this?

Yes, I'm happy to take this. So the 2 trials that we are referring to are European studies. One is TEDOVA recently presented at ASCO. And the other trial is a trial called OReO. Both trials are run in Europe and had similar patient populations because they enrolled patients with platinum-sensitive ovarian cancer and were treated in the maintenance setting. However, the patient population was not identical because the trials did not cap the prior lines of treatment. They included patients that had stable disease as well, which we don't. They also included patients who have liver metastases. And so they also could have had multiple attempts of being treated with both bevacizumab or PARP inhibitors.

So due to this, these patients were actually more heavily pretreated than our MAIA-ovarian trial. And their placebo control arm had a median PFS of 2.8 months. We anticipate that the actual benchmark is somewhere in between the historical data sets, which we took from the original registration trials for the PARP inhibitors, which was approximately 5.5 months, and these new updated trials who have a similar patient population. And therefore, we've adjusted it to approximately 4 months. As such, we currently don't know who is allocated to which arm because our trial is blinded. So we're making these adjustments based on emerging data.

And maybe I could add that eventually, we change -- the approximation is roughly around 4 months. But I think eventually, what is more -- most important for this trial is that that's why we have an internal randomized controlled placebo arm, and eventually, we are comparing COM701 40 patients treated in monotherapy versus placebo arm of 20 patients, whatever antitumor activity we see in the treatment arm is COM701-driven. It's not a combination study. And the assumptions for the placebo control are important, but eventually the critical is the actual data on the trial comparing placebo to COM701 treatment.

Okay. And then maybe just quickly on GS-0321. I guess, you've been dose escalating now for, I guess, around 18 months or so. Have you had a conversation with Gilead about presenting some of the dose escalation data before you move into dose expansion? And is it safe to assume that you are now dose escalating both in combination with the PD-1 inhibitor, and I guess, monotherapy as well?

Yes. So typically, with this kind of arrangement with pharma companies, we cannot say much. I would just remind that as you -- this said, we have dose escalation in mono and in combination with PD-1. We also have backfill course in the monotherapy, meaning more patients in the higher doses, and then, the expansion phase. So we're looking at benchmark studies in this stage. Yes, I think it's reasonable to assume that everything is moving forward as planned. That means that probably we are already doing combinations and other expansions, but -- for sure, I mean, in the backfill course, I would say. But you cannot say precisely where we are and in which stage we'll disclose data. I think it's still early. I mean, if you -- even if you look at other benchmark studies, Phase I studies, 18 months into the study, it's a bit early for reporting data.

The next question is from Leland Gershell of Oppenheimer.

Just 2 questions for me. Just wondering with respect to the MAIA-ovarian trial and the guidance for the data. Just wondering, given the nature of the kind of changing assumptions and event-driven nature, could you see to the extent possible, a readout that might come before the end of the year? And also, I want to ask, are there any particular biomarkers that you'll be looking at alongside the clinical PFS outcome future studies?

Thanks, Leland. So for the first question, we are -- yes, the PFS of the placebo is now a bit shorter, but we are not changing our guidelines. And eventually, that's why we said the results will be by Q1 '27. It is depending on the actual data on the study. And obviously, we're going to report it when the data is mature enough.

Michelle, you want to add something for the second question about the biomarkers and other readouts to look at the study?

Sure. So we're -- our primary readout is progression-free survival. We don't yet -- we don't have a specific biomarker selection strategy other than patient characteristics where we have excluded patients with liver metastases. And the other thing to note is that in our earlier data, we did see activity in patients who were both PD-L1 positive and PD-L1 negative. So other than trying to enrich for more clinical attributes, we don't have a specific biomarker, and we do have an exploratory plan that we will analyze when we unwind the data.

The next question is from RK of H.C. Wainwright.

Eran and team, this is RK from H.C. Wainwright. One quick question. Have you had any interactions with the FDA to see if the MAIA-ovarian trial alone could support either an expedited or an accelerated path for approval, especially in this setting that we don't really have a drug approved?

Thanks, RK. Michelle?

Okay. Sure. So at this point in time, we have not had a meeting with the FDA. Once the trial reads out, we will follow all the appropriate regulatory steps. What I will say to you is we incorporated a lot of the guidelines from the FDA in designing the trial, and it's definitely in line with their guidance on Project FrontRunner, which is one of the reasons why we did go into an earlier line of treatment as well as using the Bayesian trial design, which is, again, part of the FDA guidelines that have recently come out. So we are confident that with robust data, we will be able to have good engagements with the FDA.

Is it possible for me to ask another question?

Sure.

Sure.

On the partnership with AstraZeneca, now that they have 12 clinical studies going on and 12 Phase III studies going on, do you have an idea of what we should expect in terms of the earliest Phase III readout that we could see? And also, does this inclusion of the new trial, does it change either the schedule or composition of the $95 million milestone outstanding?

I will start with the second question. This doesn't change. I mean, just it's another short-term goal in a new indication in combination with ADC, which is, again, very promising, also based on what you've seen from the Phase II study. So this goes for the agreement terms.

Can you remind me the first question, please, RK?

Do you have any idea of which of the Phase III studies we could see data from and anything on either the timing? Or what data we could be seeing or from which study you could be seeing data?

So we could refer only to what AstraZeneca are saying. And while they are reporting continuously data on Phase II studies as this year in ASCO and in the conferences, the Phase III results according to their guidance is after '27, meaning '28, and no, it doesn't mean that it couldn't be earlier interim analysis and other options, but the actual formal guidelines are after '27 for the Phase III studies.

This concludes the Q&A session and Compugen's investor conference call. Thank you for your participation. You may go ahead and disconnect.

Hello, everyone. Welcome to Jones fireside chat with Dr. Eran Ophir, President and CEO of Compugen. I am Danya Ben Hail, an analyst at Jones Research.

Compugen was doing computational target discovery long before AI and biotech became a buzzword. Today, we'll explore what it really takes to turn predictive biology into first-in-class immuno-oncology drugs. Eran, thank you for joining us.

Thank you Danya for inviting.

Let's start with the foundation. Compugen repeatedly uncovers first-in-class targets where our traditional discovery methods stall. Every AI company today claims a data advantage. Getting started, can you give a brief overview on Compugen's platform and what makes it unique?

So first, as you mentioned, we are not just a recent AI story that's saying that we're doing AI, just to have the buzzword in the name of the company. We're doing it a long time ago. We have built the system. We have this engine called Unigen. And so this is one.

I think the second part is the stage of the research and development that we are focused in, which is relatively unique. I mean you gathered a really nice group of companies in this set of fireside chat with AI companies. Most of them are doing, for example, AI to identify the drug targets, to identify easier, maybe better antibodies, small molecules. But we are focusing on the very first stage of the research and development on the drug target itself, which target, which molecule, which protein in the human body we should target to really modify it to have eventually effect in cancer patients. And there are not many companies that are focusing on this relatively challenging first part of bringing novel targets.

And there are definitely not many companies that have shown again and again that they can bring novel targets and that they are generating clinical data and further validation by pharma companies collaborating on the targets. So I think this is another differentiation that the platform is validated.

And finally, is not only the AI and the machine learning and the algorithms and the database that we have that we built along years. It's really the end-to-end capabilities. In one company, we have this know-how, again, developed along years of using the right algorithm, right data sets, asking the right questions to identify the drug targets, but then also how to validate, how to eliminate targets that should not proceed, how to choose the most promising one to take into the clinic. And then in the clinic, we're exactly to take them. I think also this end-to-end approach is relatively unique for Compugen.

Yes. That completely makes sense. So I mean, you through the proprietary algorithms, your decades of accumulated wet lab and you have the specific way to map the immune evasion mechanisms. So all of that together brings it, gives you this advantage? Or is there anything very specific and unique that you would like to say this is what -- this is the point of uniqueness or...

So it's absolutely that. It's the combination of how these pieces reinforce each other. We have great algorithms. We're mapping the tumor microenvironment for years from every different angle you can imagine, transcriptomics, proteomics to try to learn about the human tumor microenvironment. But then also the convergence of disciplines, having data scientists, biologists and clinicians sitting together in the same table, asking themself what clinical problem we can solve, but asking a specific biological question and how we can use the algorithms and data science to help us identify the targets to solve that problem. So this is one.

And second is that this is a flexible approach. So the database continue and feeds itself. We continue to generate data all the time from the preclinical data, from clinical studies we're doing, we're sequencing patients. Whatever sample we can put our hands on, we're sequencing and this feeds back into the database to enable us to choose even better targets for the next round.

Yes. Given the high failure rate of novel biology, so why is finding new targets still the most valuable application of your platform? And how do you protect against the existential risk of novel target failing in Phase II?

So first, I don't think this is only a problem of a novel target, which fails in the clinic. This is -- the biggest challenge is how to really predict clinical success in the preclinical package. For example, if you want to generate a better molecule for a known target, then you need sometimes to be better than the existing one and you need to be differentiated. So you can -- even if your molecule is working because the target is validated clinically, you are not better than the existing drug.

So there are many challenges also for developing better drugs for known targets, especially, I think these days when China competition rising up, I think that really bringing the target itself and not just trying to develop better drugs on known targets is something which is still a challenge, something that we have a know-how and advantage in how to do it. And again, given the recent competition for China, I think this is still something which is unique and still is -- have less competition and less competitive pressure from others.

Yes. I mean you're right. And the industry has seen like high-profile failures. But I will point that especially in targets that looked great in silico, but failed in humans. So how does Compugen ensure its models are capturing real drug responsive human biology rather than just finding statistical noise in massive multi-omics data sets?

So this is a very important question. It has multiple layers of the way we ensure it. First of all, we are not looking into statistical noise in data sets. We are starting with a unique clinical question. And we always, always, always make our analysis in the most relevant human samples. We never use proxies. We make sure that we have the right data set of human tumors from patients to answer the clinical questions that we have. But then it's the targets that we are working on are never remains in silicon.

Then come as discussed before, the end-to-end capabilities, how to build the biological package to really convince us, first of all, that the target is a valid target that can succeed in clinical settings. So we put huge efforts into doing all the right experiments. And maybe I can take an example. the COM503 that we licensed to Gilead, it haven't yet proven clinical, at least we didn't disclose any clinical data, but at least the package was convincing enough for a few pharma companies to chase it and eventually, we got this $90 million -- $850 million deal, $60 million plus $30 million and all of that. So the package was convincing also to others, let's say that.

So the COM503, we started with a very unique clinical question about resistant mechanism to PD-1. And then we looked into patient samples in Unigen for some of the samples, we actually -- for that specific question, we collected more samples. We have a very good collaboration with hospitals in Israel, and we get every day samples from hospitals, from surgeries.

And then we made the discovery itself. So a disease relevant that source for the data in which we found the discovery. But then also the validation stage. We try to rely as much as we can on human samples directly ex vivo from patients, showing the activity of the drug in the most relevant system. Yes, sometimes mice could be relevant, but definitely, the focus should be on the human systems on a very rigorous validation and high bar for targets to move forward.

And then at the end of the day, also in the clinical settings to really use the computational tools to identify the patient that could benefit, giving all the data that we have. So I think this whole package going from discovery in human samples all the way to the clinical settings with a very strong biological package around it, experimental package is key to what we do. And this is, in a way, taking this initial in silico prediction into a target with full biology around it that is sufficient for us to move forward with.

Yes. And that gets into -- so you're one of the first companies to bring computationally discovered targets into human trials. What have regulators thought to you about how they evaluate preclinical packages that were rooted in predictive algorithms?

So from our experience, we didn't have any issues because eventually, we're not bringing them in silico package. We're bringing them the experimental package, the preclinical package, a lot of focus on safety. So the packages that generated for our computationally discovered targets had never any issues with regulators. We always had a nice path into Phase I INDs, acceptance and all of that. So if you generate the right package, the fact that the target initially was discovered in silico doesn't really matter much.

And okay. So with AI being implemented across the entire R&D path, what is the hardest biological constraint in drug discovery, whether it's tumor microenvironment complexity or immune pathway redundancy that no algorithm can simply optimize away?

So it's exactly that. I think that eventually, the ability to model the complexity of the human in our case, immune system, but in general, the immune system is extremely challenging. So what we are doing to address that, as mentioned before, we are really modeling and mapping the tumor microenvironment from every angle you can imagine, we definitely use the recent AI tools, which allows us to do things that we couldn't have done before, absolutely.

We could navigate now in this complex, huge complexity of data in a way that we couldn't have navigated before, definitely. And still, we're not in the place we can say, okay, we can push on a button and we get a target. This is a very complex system, very complex trial and error approach. But definitely, the tools are improving every day, and we definitely can do today things we couldn't have done in the past.

All right. So there is biological redundancy is something that AI probably can't fully predict today. Hopefully, we'll get better at. So does that explain your shift into looking at combination therapies like in your ERG inhibitors with TIGIT or PD-1 inhibitors? How does the platform account for these complex interactions?

So first of all, I think that in general, oncology is going into combinations. We know that a single drug can achieve, in some cases, significant effects. But in many cases, you need to combine different mechanisms. And this is, again, where Compugen fits in. We are bringing new mechanisms that could work as monotherapy, but could definitely also work in combination. For example, the biology of PVRIG, which we think is very relevant for ovarian cancer.

The focus now in the MAIA study, and we'll discuss it in a second, is on the monotherapy activity of COM701, the blocker of PVRIG that we identified computationally, but the next steps could definitely also be combinations. But this really depends on the patient population, what you can tolerate, the ability to combine.

Again, PVRIG, for example, COM701, the blocker of PVRIG has a very good safety profile. So it's relatively easy to combine. So I think combination is definitely something that is relevant. It's not necessarily for AI discovered or non-AI discovered targets.

Yes. And for PVRIG, what gave you the confidence to take it into preclinical and then clinical studies? What's in silico signals convince you to continue with that?

So first of all, yes, PVRIG identified computationally. There were no publications around it. The academical community didn't know PVRIG when they identified it, which is a good start, but definitely not the important part.

The important part that we started to explore it, we identified it has a very, very different biology, different from TIGIT completely from PD-1. So we don't only have a new checkpoint. It's a checkpoint that could have different consequences when you block it compared to other checkpoints. And this is what we saw preclinically, and this is exactly what we saw clinically.

In patients, we have seen this unique biology translating into activity. As mentioned before, we're sequencing the patients. We looked in patients treated with COM701 before, and we take biopsy also and samples after treatment. And we saw how COM701 can modulate the tumor microenvironment in a way that we think is unique to its biology.

And then also the clinical signals. We have, for example, a patient with PD-L1 negative ovarian cancer that failed all the standard of care treatment could receive. She received COM701 in monotherapy and that computational prediction prolonged the life of that patient. She will remain on the study for 2 years. So the goal of the current MAIA study is to take the signals we have seen -- I mean, so the drug is active. And PVRIG is not in silico prediction now. We know it's an active drug that could modulate and affect the progress of ovarian cancer tumors. We also have seen signals in other tumors.

And now the MAIA study is a study we are doing that after seeing signals in the last line, platinum-resistant ovarian cancer, patients who failed everything. Some of them had 10 prior lines. We are now taking the signals we have seen and a very good safety profile, into an earlier line of platinum-sensitive patients, ovarian cancer, second, third line. And the goal of the study is really to see can COM701 in monotherapy mediate significant monotherapy activity and prolong the progression-free survival of these patients who have no standard of care.

These patients have a huge unmet need in the second, third line, they receive the platinum, and there is no treatment approved to maintain them from becoming platinum-resistant, and this is the goal of the MAIA study.

And we expect interim data readout in first quarter '27 correct?

Absolutely. We expect to have the interim analysis, which will include the meaningful data progression-free survival and any other clinical signals by Q1 '27, yes.

And if the data is strongly positive, does Compugen take the leap into building its own late-stage clinical infrastructure? Or does that milestone simply trigger another out-licensing event?

Yes. It's a good question. It will depend on the actual data, magnitude of effect, whether we will think that -- remember, again, there is a huge unmet need. So definitely thinking about this exact patient population and now we can go to registration fast will be the first priority, either we can do it alone or maybe we think that the best thing will be to partner to move fast and aggressive into Phase III.

In addition, we're talking about an adaptive trial design. So we can also add additional arms to continue to explore the possibilities. For example, we can combine COM701 after showing the monotherapy with bev, we can combine it with ADCs and then open also more opportunities going earlier, later in ovarian cancer and also into other indications.

Yes, especially taking into account it's a very competitive space right now.

It's a very competitive space, but there are very few nontoxic agents, which are fighting for that space. And patients after 6 cycles of platinum, some of them may want to have a bit of an easier drug than an ADC, which is eventually toxic. And the pharma companies, which are fighting between themselves with the different ADCs also want a way to differentiate. So having a combination partner, which is combinable and ideally, again, the durability we have seen in the last line will translate here as well could also be a matter of priority for -- to differentiate in the competition. for pharma companies.

Yes. Makes complete sense. You've secured impressive validation with your AstraZeneca and Gilead partnerships, bringing in substantial milestone potential. Is the monetization strategy to continue offload these assets early? Or yes, so do you intend to keep full commercialization right for future discovery assets beyond what you have currently in the pipeline?

So I think it's really going to be program dependent. First of all, I think with the financial stability we have now after the monetization of a small portion of the AstraZeneca royalty last year. So we now have cash in '29. So we have financial stability, and this gives us the freedom to make our choices because we don't have to rush and out-license necessarily to maintain the company alive.

So if we think for a specific program, if we generate additional data in a Phase II or maybe even a Phase III study, if it's a small and focused one, we will bring most of the value for ourselves and for the shareholders, we'll do so. If we think that we need now a very aggressive clinical program, and we need a pharma partner to move aggressively in multiple fronts, and this will be the path that will bring most of the value to the company and our shareholders. This will be the path. eventually it's going to be program dependent.

Yes. And to summarize this part, so where does your platform create the sharpest shift in return on investment? So is there financial and operational leverage found in accelerating early target discovery? Or is it derisking downstream clinical decisions? Where is it at?

So I think, first of all, the platform is focusing on bringing new biology, bringing new targets. As mentioned before, pharma companies tend to hear -- also biotechs to hear around the same target, same biology, and we're bringing new biology that could really enable more new options for patients.

But also as discussed, the rigorous process that we are doing, and this is yet to be proven, but I think this is ongoing, should bring us not only targets with new biology, but also targets we have more probability of success. We discussed before the COM701 data, and we have the readout by 2027. We didn't discuss, for example, TIGIT. TIGIT is an example of target we identified a long time ago, definitely multiple failures for TIGIT.

I think this is a case of a target that is definitely clinically active. It's clear that TIGIT is active. We've seen it in multiple trials, but some of the initial assumptions that some of the drug makers had on TIGIT maybe overestimated the activity, maybe didn't choose, in this case, the right format.

In this case, for example, I think that with the right format with the bispecific antibody of AstraZeneca, they will leverage also the TIGIT biology that we initially identified. We have 11 Phase III trials ongoing. It was interesting to hear AstraZeneca's management in the recent ASCO event talking about the way they see the evolving data for rilvegostomig.

They talked about stabilization of the responses. They showed in ASCO durable responses in early trials. They talk about combinability. So I think that also TIGIT, which is a target that we identified and had definitely a roller coaster of ups and downs. I think that AstraZeneca with their way of developing it, the clinical strategy, the bispecific will also eventually make the most potential of this TIGIT computational discovery.

Can you just highlight the differences of your TIGIT asset compared to the prior failures, just to clarify to people listening in.

Absolutely. It's very important. So again, this is an example in which doing what we think is the wrong drug format could make a difference. So most of the initial developers who develop TIGIT has an Fc active. I will not go through all that biology, but that was -- we think was not the right format. It caused safety issues. It had challenges to combine.

And eventually, it was difficult to keep patients for a long time on the study because of the safety. But even maybe more importantly is the fact that AstraZeneca are the only ones for developing TIGIT as a bispecific for PD-1 and TIGIT. This has some mechanistic advantages that we see for other bispecifics as well that could be more active and there's some evidence for that, could be more active than PD-1/TIGIT combinations that done -- others have done.

And this also allows a different clinical strategy, much easier to combine, less burden of showing contribution of components of the bispecific. So I think it's the format of the antibody, the clinical design strategy and the combination around all these 11 Phase III trials, most of them or many of them with ADCs that will put AstraZeneca's TIGIT antibody in -- which is partnered from us, obviously, in a different position than the other TIGIT were.

Yes. Thank you for that. So as we look into the second half '26 and beyond, what are the most important clinical and strategic milestones investors should be watching?

So first, obviously, is our own asset, COM701, the MAIA study by Q1 '27, we're going to have the meaningful data to show if COM701 can really drive monotherapy activity in this population of ovarian cancer.

Rilvegostomig, the expectation from AstraZeneca for Phase III readout, which is going to be the meaningful one is after '27. But we see all the time accumulation of data like in the recent ASCO showing again the durability, the safety, the potential of different combinations. So I think with the accumulation of data, it will show eventually that this molecule of TIGIT is doing something else.

And then obviously, the COM503 called now GS-0321 that we licensed to Gilead. We're already in the clinic for more than a year now and the progress through Phase I. We don't have yet disclosure for exactly when, typically when working with the pharma company, but definitely keep an eye for the COM503 readouts and the early pipeline, the computational discovery platform, we have financial stability. We have a validated engine that we will continue every day to leverage and bring more assets. And along the coming year, again, we don't have specific guidelines, but definitely, we will report on the early pipeline when time will come.

Great. Looking forward. So to close up, we'll do a rapid fire questions section. So let's get going. Most overhype claim in AI drug discovery today.

I think that people that say that AI is going to dramatically increase clinical success rate in cure any disease are still a bit early. Things are moving fast, so difficult to make predictions. But for now, human system is too complex to be solved with a push of a button.

So most underappreciated bottleneck?

The clinical development. The community must do something, especially in the U.S., but also in general about making trials cheaper, faster. We have great targets. We need to test them. We need to see in patients if it works or not. And for that, we need a better system for faster and more cost-effective clinical development process.

And hopefully, I can help with that.

Absolutely.

What is the one metric investors should focus on that actually captures platform value?

So eventually, looking at the totality of the assets that we have and that we will have and we will disclose our ability to open new target space, new mechanism to bring additional BD activities to bring more clinical validation for our internal and partnered assets.

One proof point investors should demand over the next 2 to 3 years?

Eventually, the proof is in the pudding. I can sit here and tell about the processes we are doing and the rigorous validation. Eventually, an asset should show success in clinical translation. This is what we work for. This is what the investors should wait for.

Great. Well, thank you for the thoughtful discussion. What you've built at Compugen shows that computational biology isn't about shortcuts. It's about uncovering biology that was invisible to traditional methods, and we are looking forward to the future updates.

Thank you, everyone, for joining us today. Enjoy the rest of the upcoming sessions.

Thank you, Danya.

Ladies and gentlemen, thank you for joining us today. Welcome to Compugen's First Quarter 2026 Results Conference Call. [Operator Instructions] As a reminder, today's call is being recorded.

I will now hand the call over to Lindsey Trickett, Head of Investor Relations and Corporate Communications to begin. Lindsay, please go ahead.

Thank you, operator. Good morning and good afternoon, everyone, and welcome to Compugen's First Quarter 2026 Financial Results Conference Call. With us today are Dr. Aron Ofer, President and Chief Executive Officer; David Silverman, Chief Financial Officer. Dr. Michelle Miller, Chief Medical Officer, will join us for the Q&A portion of the call.

Before we begin, I'd like to remind you that during this call, the company may make projections or forward-looking statements regarding future events, business outlook, development efforts and their potential outcome, the company's discovery platform, anticipated progress and plans results and time lines for our programs, including disclosure of clinical data, financial and accounting-related matters as well as statements regarding our cash position and cash runway. We wish to caution you that such statements reflect only the company's current beliefs, expectations and assumptions and that actual results, performance or achievements of the company may differ materially. These statements are subject to known and unknown risks and uncertainties, and we refer you to our SEC filings for more details on these risks, including the company's most recent annual report on Form 20-F. The company undertakes no obligation to update projections and forward-looking statements in the future.

With that, I'll now turn the call over to Dr. Erin Ofer, President and CEO.

Thank you, Lindsay. And good morning and good afternoon, everyone. Before I turn to our business update, I want to take a moment to formally welcome Lindsay, our new Head of Investor Relations and Corporate Communications to Compugen. Lindsay joined us with strong experience in Investor Relations, and we are thrilled to hover leading our communication with the investment community. Welcome, Lindsay, and we're glad to have you on board.

Now let's start with our business update. 2026 is shaping up to be a significant year for Compugen, and I'm pleased to share our progress in the first quarter of 2026 as we continue executing on our strategic priorities. Starting with our fully owned clinical program, COM701, a potential first-in-class antibody target PVRIG, which is an immune checkpoint with unique biology much differentiated from other checkpoints, including PD-1 and agent. We believe this unique biology underlies the clinical activity demonstrated for COM701 in less inflamed indications such as ovarian cancer.

As a reminder, at ESMO last year, represented the full analysis of clinical data showing that COM701 in monotherapy and combinations was well tolerated and showed consistent, durable responses in patient with heavily pretreated platinum-resistant of ovarian cancer. Based on these results, we decided to progress the development of COM701 and test it in earlier settings of ovarian cancer as a maintenance therapy in patients with relapsed platinum-sensitive ovarian cancer that responded to their most recent line of chemotherapy.

The rationale is to allow COM701 to induce its antitumor activity in early relying patients with lower tumor burden, less compromised immune system and by that, increase the likelihood of these patients to benefit for COM701 unique mode of action. For this purpose, we initiated the marioviroAdaptiv platform trial. In such study 1 of this trial, Comsebralis randomized is maintenance monotherapy versus placebo in patients with relapsed platinum-sensitive or bearing cancer. We're actively enrolling patients in clinical sites across the United States, Israel and France.

Having all sites open and enrolling, spanning leading academic centers in U.S. and Israel, as well aside from the cage Ginko French corporative group gives us confidence in our ability to complete enrollment on schedule for having the Mivan median PFS data at interim analysis by Q1 2027.

This patient population comprised of those progressing post PARP inhibitors and/or EM overall lot candidates for sustreatment represent a significant unmet medical need with no current standard of care. We believe that clear prologation of PFS in these patients could inform a registration task for COM701 and make it a potential backbone for drug combinations in this population while also enabling a potential broader clinical development plan across earlier and netilize of ovarian cancer treatment as well as in other indications for clinical signals previously seen for COM701.

In addition, we're happy to see our partner AstraZeneca's progress on their broad rilvugosomic program. We remain confident in real potential based on its differentiated bispecific antibody formats in addition to clinical and combination strategies. Last month, AstraZeneca presented multiple abstracts featuring yield at the AACR Annual Meeting in San Diego, reinforcing our confidence in the differentiated design and growing potential. This includes preclinical data demonstrating potential opportunities for Velvet as an IO backbone for combination and also laboring data from the Destiny gastric 3 Phase II trial evaluating relevant combination with the blockbuster ADC and HER-2 and chemotherapy as first-line treatment for HER2-positive gastric cancers. These data showed promising antitumor activity and also demonstrated combinability of real from a safety perspective.

Overall, these ACR publications continue to reinforce our confidence in Relday as AZ continue to advance it along 11 Phase III trials across multiple indications, including the recently opened trial in gastric in combination with the closing 18.2 ADC.

With that, we are looking forward to the release of additional clinical data along the year, including at the next ASCO meeting at the end of the month. As a reminder, AstraZeneca's previously estimated a nonrisk-adjusted peak annual revenue potential of more than $5 billion per Wheeler and were eligible for additional $95 million in future regulatory and commercial milestone payments plus mid-single-digit tiered royalties on sales.

Moving to GS-0321, formally known as Confio, our potential first-in-class anti-IL-1 binding protein antibody licensed to Gilead. GS-0321, a novel antibody approach to any cytokine biology for the treatment of cancer, potentially overcoming the limitations of direct cytokine administration. The ongoing Phase I dotscalation trial continues to progress as we planned. As a reminder, we received to date $90 million from Gilead of this asset, on eligible to receive up to $758 million in additional milestone payments plus up to double-digit tildalties.

Now to the early-stage pipeline, and enogen discovery engine. Beyond our clinical assets, we continue to invest in our early-stage immuno-oncology pipeline. UNIGEN our AI-powered computational target discovery platform has already discovered the targets of COM701, COM902, NGS. We remain committed to identifying and advancing the next wave of innovative programs, grounded in novel mechanism of action designed to activate the immune system against cancer. Importantly, we have a solid financial position with a cash runway expected into 2029 following the December 2025 transaction with AZ, through which we received $65 million in nondiluted capital by monetizing only a small portion of our future rebroalties.

Our financial stability allows us to fully focus on advancing our pipeline and reaching key value-creating buystones with both our internal and partnered programs. And throughout all of this, we continue to benefit from a deeply talented and highly committed tumor Compugen I am proud of what we have built and energized but opportunities ahead.

With that, let's hand over to David for the financial update before we open the floor for Q&A.

Thank you, Evan. And I would like to add my own warm welcome to Lindsay as well. It is a pleasure to have you join the Compugen Ltd. and Team Lindsey, and we look forward to working together. I am pleased to say that we continue to advance in 2026 with a solid balance sheet and financial flexibility. Cash runway, assuming no further cash inflows is expected to fund our parity plans into 2029. We anticipate using this runway to continue advancing our COM701 platinum-sensitive ovarian cancer trials, may ovarian and to support the progression of GS-0321 in the clinic, together with continued investment in our early-stage pipeline.

Now going into the details, I will start with our cash balance. As of March 31, 2026, we had approximately $134.9 million in cash, cash equivalents, short and bank deposits and investments in marketable security. Revenues for the first quarter of 2026 were approximately $2.2 million compared to approximately $2.3 million of revenue for the comparable period 2025. The revenues in the third quarter of 2026 and 2025 reflects the recognition of posted of both the upfront payment and the IND milestone payments from the license agreement with inlet. Expenses for the first quarter of 2026 were in line with our plans. R&D expenses for the first quarter of 2026 were approximately $6.9 million compared to approximately in the first quarter of 2025.

The increase is mainly due to an increase in clinical expenses related to my ovarian trial as well as higher drug supply costs supporting our trials. Our G&A expenses for the first quarter of 2026 were approximately $2.3 million compared to approximately $2.4 million for the comparable period 2025. For the first quarter of 2026, our net loss was approximately $7.7 million or $0.08 per basic can be look a share compared to a net loss of approximately $7.2 mill or $0.08 per basic and diluted share in the first quarter of 2025.

With that, I will hand over to the operator to open the call for questions.

[Operator Instructions] The first question is from Lana Grab of [indiscernible] Partners.

Thank you for the question. Lindsay, welcome. Nice to see you here. Going into ASCO, I wonder if you could talk about more specifically the data sets going to prevent witruvagostimig? And helps set the context for what we should expect to see? And are there benchmarks that would -- that we should be keeping in mind when we review the data set?

Sure. Thanks, Dana. So we're talking about 2 DAS assets, clinical data. Obviously, the actual data is not released yet, and I would be cautious on setting expectations AstraZeneca but over, we talk about on the I-SPY trial in the testing will be cost to me in elegant settings with Synet, which is by itself a blockbuster drug, which is very exciting to see these combinations. .

Again, I would be cautious about the expectation. But I think looking again, and this is a platform trial, so really trying to look across the nutrandomize study, but trying to look about driver versus other data sets. The combinability is again going to be very important and to show again how the Fc reduced format of rivagostamig is easy to combine with such ADCs.

And then the second set is the Gimi which is in combination with chemotherapy. And here again, we'll be good to see. I think it's a bit of a longer follow-up from what was reported before. So we to see about the long-term effect of the PSS -- I'm not sure if there will be an OS data, but how the long-term effects are shaping, including the long-term safety in combination with chemo, having in mind that there is -- for this trade, there's an ongoing Phase III study ongoing. So I guess the comparison to sterocontrol should be with caution and still probably is going to be made.

The next question is from Stephen Wiley of St.

Maybe you can just talk a little bit about how you're thinking about disclosing future development candidates that are discovered off the Inogen platform. I think the IL-18 binding protein antibody wasn't announced until it was ready for clinical development. Is that kind of how we should expect incremental assets to emerge out of the pipeline once they're ready for an IND submission?

Thanks, Steve. So I think it's really dependent. Eventually, definitely, the biggest group in Compugen is the 1 that continue to work to bring additional innovative assets like COM, which is called today 031 -- specifically for that asset, it was right for this asset and for Compugen at these times to out license it in the clinical stage. So this also influenced the stage in which we disclosed it. It was relatively early. But it doesn't mean necessarily that we have any specific guidelines that we are porting on early assets only when it's ready for IND or only on its election. It really depends on the actual assets on the stage of derisking in which you want to start comment and committing.

So again, I wouldn't learn too much from the story filing by the protein other than the fact that it was another demonstration of our competition platform can bring such innovative approaches in that case, not only first-in-class asset, but the first-in-class approach to highlight cytokinebology for equites cancer and we are looking into different MOAs not necessarily similar to that to bring again another innovative options that could really make difference to patients.

The next question is from Renan GershofOpeneier.

Wondering if -- could you remind us if the ovarian trial, is that stratifying for patients who are PD-L1 or PD-1 expression status. And I also want to ask when we see the interim data in the first quarter, will given that this is an adaptive trial, would that mean that the interim data could inform some change your design? Or would you simply keep going as planned?

Thank you, Live I think Michel can take this one. .

I think to take this one, yes. So the mylovarian trial actually is not stratified according to PD-L1 subgroup. We are stratified by second versus third-line treatment. And in '17. When a result, we have multiple options ahead of us in terms of adjustments to the trial. So we would consider adding additional arms and a lot of it's going to depend on the totality of the data and also plans towards engaging with the regulators and steps towards a pivotal trial.

Equal additional comment a little about the PDL1 certification, I would like to remind you that FIBRA probably because it's unique biology, we saw in other indications, specifically in ovarian cancer, we saw responses at pro-PD1-pst and PD-L1-negative patients. So for now, we didn't see not necessarily like for other checkpoints that the PD-L1 subset is the 1 responding to COM701. And again, I think this is because that unit biology, very much differentiated from PD-1 so again, not necessarily PD-L1 certification here.

The next question is from RK of H.C. Wainright.

So a couple of more questions on the ovarian cancer trial. So now that you have all these sites active, what is -- any commentary on the enrollment status itself and also because this is an event-driven trial, and any commentary on required events that needs to happen for the interim analysis? And the third question is, what -- what are you assuming for the control on PFS? And what sort of hazard ratio do you need to see to consider that as a win?

Michel, do you want to take .

Yes, sure. So firstly, with respect to enrollment, we're not commenting at this point in time, but I will say to you that we are on track our interim analysis as planned in the first quarter of 2027. And our participating investigators have a high level of engagement and are working really well with us. Regarding the events and the benchmarking. So the trial is an exploratory trial. And so at this point in time, we don't know the full magnitude of benefit, but the benchmark for the control arm from prior clinical trials in the second line and third line of maintenance in those trials where patients did not get treatment. The same patient population had a benchmark of approximately 5.5 months, although there was a range. So in some studies, it was as low as 3.8 months and others as high as 5.8 months. we're hoping to be able to show that there is meaningful single-agent clinical activity of COM701 and we've hypothesized that we would like to see a 3-month or greater improvement of the benchmark PFS.

This concludes the Q&A session on Compugen's investor conference call. Thank you for your participation. You may go ahead and disconnect.

Ladies and gentlemen, thank you for joining us today. Welcome to Compugen's Fourth Quarter and Full Year 2025 Results Conference Call. [Operator Instructions] As a reminder, today's call is being recorded. Participants from the Compugen team are Dr. Eran Ophir, President and CEO; and David Silberman, Chief Financial Officer. Dr. Michelle Mahler, Chief Medical Officer, will join for the Q&A. Before we begin, we would like to remind you that during this call, the company may make projections or forward-looking statements regarding future events, business outlook, development efforts and their potential outcome, the company's discovery platform, anticipated progress and plans, results and time lines for our programs including disclosure of clinical data, financial and accounting-related matters as well as statements regarding our cash position and cash runway.

We wish to caution you that such statements reflect only the company's current beliefs, expectations and assumptions, but actual results, performance or achievements of the company may differ materially. These statements are subject to known and unknown risks and uncertainties, and we refer to you our SEC filings for more details on these risks including the company's most recent annual report on Form 28. The company undertakes no obligation to update projections and forward-looking statements in the future. With that, I now turn the call over to Eran.

Thank you, operator, and welcome to everyone joining our call today. On today's call, I would like to highlight some of our key achievements in 2025 and outline our planned strategic priorities for 2026. During 2025, we made progress across our business scientifically, operationally and financially, including the following key highlights.

We extended our expected cash runway into 2029, assuming no further cash inflows through a nondilutive transaction with AstraZeneca tied to relive their differentiated PD-1 TIGIT bispecific, the digit component of which is derived for COM902, our fully owned Fc-reduced anti-TIGIT antibody. We also diversified our leadership team as I stepped into the CEO role in September 2025 and not transition to Executive Chair.

On the clinical side, we are on our clinical programs initiating new clinical trials with our wholly-owned potential first-in-class anti-PVRIG COM701 and our potential first-class anti-IL-1 bilingprotein antibody GS-0321, lesser to Gilead. We also advanced our clinical footprint, opening sites in the U.S., Israel and France in our COM701 clinical trial. In addition, represented clinical updated ESMO and SITC conference for COM701 and GS-0321, respectively.

So let me elaborate on each of these highlights, starting with the most recent update our December 2025 strategic transaction with our partner, AstraZeneca, where we monetize a small portion of our future relive royalties to AstraZeneca. This deal is important today and for the long term because -- it added $65 million in upfront nondilutive capital from AstraZeneca, extend our expected cash runway into 2029.

It provides an additional $25 million at the next milestone payment which is BLA acceptance and thereby increases our total remaining milestones to up to $195 million for around $70 million previously. And we retain the majority of our royalty interest levering our economics fundamentally intact. So both before and after the deal, we remain eligible for up to mid-single digit tiered royalties from real bests. We believe this deal allowed us to unlock value today to continue advancing our innovative immuno-oncology pipeline, including COM701, GS-0321 and our early-stage pipeline and it allows us to reach both internal and partnered catalysts.

All of this without compromising our long-term upside in Relay, a potentially multibillion-dollar assets. And to put this into context, rilve is being advanced by AstraZeneca, a broad late-stage development program, including 10 active Phase III trials. AltraZeneca, previously estimated a nonrisk-adjusted peak annual revenue potential of more than $5 billion for rilve.

Next, let me briefly touch on the leadership transition. I'm excited and privileged to have had the opportunity to step into the role of President and CEO in September 2025. With Anano serving as Executive Chair, we believe we had a leadership structure that combines operational focus and strategic continuity, a strong foundation for Compugen next phase of growth.

Turning now to clinical execution, starting with COM701. In the myOranclinical trial, in the platinum-sensitive ovarian cancer, we initiated dosing and expanded our trial footprint globally by opening trial sites in the U.S., France and in Israel. I also want to highlight the data we presented at ESMO last year from the Cove pooled analysis of Phase I clinical data in platinum resistance ovarian cancer. The pooled analysis demonstrated that Comseveran was well tolerated and showed consistent, durable responses in patients with heavily pretreated platinum-resistant ovarian cancer, particularly in those without liver metastasis, representing patients with oral disease burden and potentially less immunosuppressive tumor macroenvironment.

We believe this data support the rationale for advancing COM701 in the early line settings as maintenance therapy in platinum-sensitive ovarian cancer. These programs underscore our commitment to pioneering innovative biology. Regarding GS-0321, our partner program with Gilead, we initiated dosing in a Phase I dose escalation and expansion trial and subsequently presented a trial in progress update at CIT.

Overall, we believe that our achievements in 2025 set the stage for continued execution in 2026, which transitions me nicely to our 2026 strategic priorities, which includes the continued execution of the MAIA-ovarian conductive trail. The first HAP trial is a randomized trial, comparing COMSEvoRan monotherapy to placebo in the maintenance setting of platinum-sensitive ovarian cancer, a setting where there is a significant unmet medical need and no current sort of care.

We are on track to have an interim analysis in Q1 2027. This data could lead to maintenance monotherapy past registration and for a potential bedbone for drug combination in this population. We're also enabling potential broader clinical development plan across ovariccancer lines of treatment and in other indications or clinical signals were seen for COM701. In parallel, we're executing on our Phase I trial with GS3 as a reminder, the first pressure was dosed in January 2025. GS0321 is our potential first-in-class anti-IL-13 binding protein antibody licensed to Gilead.

We believe that the key differentiator of GS-0321 is that it is not a cytokine, but an antibody harnessing cytokine biology for the treatment of cancer. It's new in a cool mechanism and venoclinical data this approach by offer advantages on both safety and efficacy. Gilead has already paid $60 million upfront and an additional $30 million when it successfully achieved IND clearance, we're eligible to receive up to additional $758 million in future milestones and single-digit to low double-digit tiered royalties.

The ongoing Phase 1 constitutes 2 parts: Part 1, dose escalation and Part 2, motivation. In addition, we continue to track our partner AstraZeneca's progress very closely as they execute on their broad Phase III relay program. Given the recent history in the TIGIT field, it's worth taking a moment to explain why we maintain confidence. For us, the answer is clear, antibody format matters, and clinical and combination strategy.

So let me explain. On format, relve is an anti-PD-1 TG bispecific antibody that has the reduced FC functionality. This design delivers coordinated inhibition of both PD-1 and TIGIT on the same immune effector cells with cooperative binding, resulting in greater efficacy, the anti-PD-1 plus anti-TIGIT single combinations when tested in ex patients derived models of non-small cell and pence. In addition, this format using reduced safety functionality maybe reduce the unwanted depletion of immunofactor cells and maintain a favorable safety profile.

In vehicle, AstraZeneca trials are designed differently from some other companies digital, and also include novel combinations like ADCs that have not been tested thus far. So to summarize, our confidence in relve is based on its differentiation at different drug formats in a different clinical trial and combination strategy.

Lastly, turning to our early-stage pipeline. With our current cash runway expected into 2029, 2026 will be our continued focus on our early stage pipeline, which is managed by the largest team within Compugen. UNIGEN AI machine-based computational engine that generated COM701, CO09022, NGS-0321, and we remain committed to investing in this differentiated discovery platform.

So stepping back, let me summarize where we are today. We have a unique positioning, solid financial outlook that enable us to continue and leverage our computational drug target discovery engine to deliver the next generation of novel immuno-oncology assets. We have a clinical pipeline grounded in potential first-in-class immuno-oncology science, and we have 2 validating partnerships with AstraZeneca and Gilead representing approximately up to $1 billion in potential milestones plus royalties.

And our team is consistently striving to deliver at the highest levels. I'm incredibly proud of what our team has delivered and equally excited about the opportunities ahead. Thank you to everyone at Compugen for dedication. With that, let me turn it over to David for the financial update before we open the call for questions.

Thanks, Eran. I am pleased to say that we are advancing in 2026 with a solid balance sheet. Cash runway, assuming no further cash inflows is expected to fund our operating plan into 2029, and we anticipate using this runway as planned to advance our COM701 in the powering cancer trial, myaovarian and to support the progression of GS0321in the clinic together with continued investment in our early-stage pipeline.

Going into the details, I will start with our cash balance. As of December 31, 2025, we had approximately $145.6 million in cash, cash equivalents, short-term bank deposits and investments in marketable securities. The cash balance at the end of 2025 included the $65 million upfront payment from AstraZeneca for the monetization of a small portion of regarding future royalties. On the revenues front, we reported approximately $67.3 million in revenues for the fourth quarter of 2025 and approximately $72.8 million for the year ended December 31, 2025, compared to approximately $1.5 million and $27.9 million in revenues for each of the comparable periods in 2024.

Revenues for 2025 include the upfront payment of $65 million from AstraZeneca and a portion of the Avon payment and the IND milestone payment from the license agreement with Gilead while the revenues for 2024 reflect a portion of the upfront payment and the IND milestone payment from the license agreement with Gilead and the $5 million clinical milestone payment from AstraZeneca.

Moving to expenses. R&D expenses for the fourth quarter of 2025 and for the year ended December 31, 2025, were approximately $5.5 million and $22.8 million, respectively, compared with approximately $5.9 million and $24.8 million for the comparable period in 2024. The decrease in 2025 was mainly due to lower clinical expenses resulting from winding down prior clinical trials, partially offset by an increase in clinical expenses related to the May variant trial initiated in 2025.

Our G&A expenses fourth quarter of 2025 and for the year ended December 31, 2025, were approximately $2.1 million and $8.9 million, respectively, compared with approximately $2.2 million and $9.4 for the comparable periods in 2024. Finally, on net profit. For the fourth quarter of 2025, we reported a net profit of approximately $56.8 million or approximately $0.60 per basic and diluted share compared to a net loss of approximately $6.1 million or approximately $0.07 per basic and diluted share in the comparable period of 2024.

Net profit for the year ended December 31, 2025, was approximately $35.3 million or approximately $0.38 per basic and diluted share compared with a net loss of approximately $14.2 million or approximately $0.16 per basic and diluted share in the comparable period of 2024. With that, I will hand over to the operator to open the call for questions.

[Operator Instructions] The first question is from Diana Graybosch of Leerink Partners.

This is [ Raviv ] on for Dana. First question I would have is, can you help us level set on what to expect in the 1Q '27 update with COM701 in terms of what we expect to see in that update? And then the follow-up to that is, can you help us understand the time line of what is required for that path to registration that you mentioned in the call.

Michelle, do you want to take it? .

Sure. I'm happy to take it. Thanks for the question. So the current trial is an adaptive trial design, and we anticipate that there will be data maturation in 1Q of 2027. And regarding the time line and what we'll be requiring for registration is really depend on the totality of the data. And we are planning for success and would have to consider other subsequent plans or trials which we are still in discussion. -- at that point in time, ready to disclose.

Yes, I think we can say a high level, as we said in the past, that there are a few opportunities here. I mean 1 is to continue if the data indeed is -- has meaningful clinical clinically, we can continue to pass for the trace monotherapy. It can open a path for combination strategies in that population. And of course, because we know that we have signal also in broken under education, a positive monotherapy signal in this trial also opened many other options. But I guess our first steps to be in that specific population following a positive results. .

The next question is from Josh Nickerson of Stephen. Please go ahead.

This is Josh on for Steve. Could you just remind us the cadence of potential outlying milestones for rebogostomag? And maybe just provide some color on the next trigger for milestone payment upcoming.

David, do you want to take it? .

Yes, sure. Joe, thank you for the question. Yes. As a reminder, so we did the deal is AstraZeneca in December, and we disclosed our next milestone with BLA acceptance on which we will be entitled to national $25 million on top of what we are already entitled to. So going forward, we will still be entitled to EUR 195 million in milestone from AstraZeneca the rilvegostomig deal. .

We are having some technical difficulties, just a moment please. Eran, Can you hear us? .

Absolutely. .

Maybe the speakers just disconnected. We'll move to the next question. The next question is from Swayampakula Ramakanth of H.C. Wainwright.

This is RK from HC Wainwright. So trying to think through the OVARIAN trial, previously you had stated you will have some interim analysis done in the second half of now it's moved to the first quarter of 27%. Just trying to understand the shift, is it -- is it more because you're adding additional centers? Or is it because you'll see a slower accumulation of events than what you initially modeled for.

Thanks, RK. So we reported that shift already in the previous quarter. And the reason back then was a bit slower. By the way, it's not only Compugen issue, but again, for us, it was a bit slower opening of the major academical U.S. sites, which we're very glad that now all of them are open. Actually, now all the sites are open, all 28 sites are open. We mitigate for that, gladly, we were approached by the Kajanio Group, which I actually have experience in very -- in that specific patient population. And they approached us to contribute to the study.

So gladly, they joined as well. We now have all the sites open fully on track to have the readout in Q1 27. Obviously, like in any trial, we need to see that the events are cumulating as expected. But other than that, everything is on track, and we continue to be in Q1 27 as we report also in the last quarter. So no change in this quarter For that. .

Okay. And then in terms of the AstraZeneca relationship, obviously, the recent monetization speaks to the alignment to the deep alignment that AstraZeneca wants to have with the drug? Are there any discussions of expanding the use of the COM902 derived jet in additional multispecific pharmas within the AstraZeneca portfolio.

So AstraZeneca are controlling givagostomig. We don't discuss with them the on plan. I mean we did see recently that -- and this is again, I think, illustrating the commitment for the program, we did see recently a new Phase III to now in gas treatment combination with coding ADC, which is now in clinicaltrial.gov. So this would be when it's activated the 11 Phase III trial.

So they are expanding with rilvegostomig. It's not specifically COM902, but sort of a custom which contains comment for comment too specifically, we fully own it. And obviously, it's a different opportunity that you can leverage in other collaborations, probably AstraZeneca with the Rivagostomig, that will move with that 1 and not with comment. And then the last

Last question for me is on the 0321. In terms of the data that's expected, would that be in any of the medical conferences or where would we see that data? And will we see more than just initial safety.

So -- we initiated the first patient was dosed at the beginning of 2025. By our agreement with Gilead, obviously, when we report data, it has to be fully aligned with them. For now, we don't have guidelines. But typically, and also I think what Gilead will do themselves is to report it in a scientific conference. And typically, it will include activity plus safety. But for now, we are not making any commitment because it will need to be in line with with Gilead.

The next question is from Leland Gershell of Oppenheimer.

I'm just wondering as we await the update on 701 in about a year from now, first quarter of '27. Just wanted to ask what you may plan to be presenting at the various oncology meetings this year, ESMO, SITC and so forth. Can you give us a flavor of what we might see out of Compugen through '26.

So overall, from what we currently disclosed and obviously, a long deal we might update it from what we currently disclose, we -- for the Gilead has just mentioned, we don't have any specific guidelines, but it could be a long medical conference along the year. AstraZeneca and again, it's AstraZeneca program and Atrzadecision, but they do have some clinical readouts this year and they might report it in some of the static conference. I didn't disclose yet when. And this is basically what disclosed for this year and obviously, next year would be the myStudyrit, which is an important one. .

This concludes the Q&A session in Compugen's Investor Conference Call. Thank you for your participation. You may go ahead and disconnect.

Ladies and gentlemen, thank you for joining us today. Welcome to the Compugen Third Quarter 2025 Results Conference Call. [Operator Instructions] An audio webcast of this call is available in the Investors section of Compugen's website, www.cgen.com. As a reminder, today's call is being recorded. I would now like to introduce Yvonne Naughton, VP, Head of Investor Relations and Corporate Communication. Yvonne, please go ahead.

Thank you, operator, and thanks, everyone, for joining us today. Here with me from Compugen team are Eran Ophir, our new President and CEO; and David Silberman, our Chief Financial Officer. Michelle Mahler, our Chief Medical Officer, will join us for the Q&A. Before we begin, we would like to remind you that during this call, the company may make projections or forward-looking statements regarding future events, business outlook, development efforts and the potential outcome, the company's discovery platform, anticipated progress and plans results in time lines for our programs, including disclosures of clinical data, financial and accounting-related matters as well as statements regarding our cash position and cash runway.

We wish to caution you that such statements reflect only the company's current beliefs, expectations and assumptions, but actual results, performance or achievements of the company may differ materially. These statements are subject to known and unknown risks and uncertainties, and we refer you to our SEC filings for more details on these risks, including the company's most recent annual report on Form 20-F. The company undertakes no obligation to update projections and forward-looking statements in the future. With that, I'll turn the call over to Eran.

Thanks, Yvonne. Good morning and good afternoon, everyone. I'm delighted to speak with you today as Compugen's new President and CEO. I'm really energized stepping into this role as such pivotal time for our company. Having led our scientific strategy in my forward position as CFO, I've seen firsthand how our science has evolved, and I believe we can deliver significant value for patients. So where do we stand today. Our fundamentals are strong and our strategy is clear. We are pioneers in computational drug target discovery. And we believe that our deep expertise in TIGIT biology is now gaining clinical momentum. I think that now it's a great time to highlight what makes us different in the TIGIT drug development space and why you should be paying close attention to our differentiated Fc-reduced anti-TIGIT programs and their advantages over Fc-active anti-digital antibodies. Reflecting on the history of drug development, one can appreciate that indeed choosing the right therapeutic target to cure disease is critically important.

But choosing the right drug format, which fits that specific target is just as important. We know that anti-TIGIT antibodies with the Fc-active format have not lived up to expectations. And most of these programs were discontinued. However, this did not surprise us because Fc-active anti-TIGITs can deplete TIGIT positive effect on T cells and T regs. This is not desired because 1 on efficacy. TIGIT is present on effector T cells. So similar to the action of anti-PD-1s -- invigorate these exhausted cells and avoid their depletion Two, on safety, TIGITs present on Tregs depleting peripheral there could result in immune-mediated side effects.

Fc reduced anti-TIGITs like our own COM902 in contrast, preserve and reinvigorate the factor T cells avoid depletion of peripheral Tregs and therefore, have the potential for improved immune activation and a better safety profile. It is notable that as earlier Phase II trials with Fc-active anti-TIGITS, safety was a concern with high rates of discontinuation due to sevens. This was also even more evident in the Phase III trials. For example, during the recent ESMO meeting, the presenter highlighted that TRPR-07 trial, adding Fc-active TIGIT to atezo resulted in these patients only receiving bid number of doses of 12 versus 17 in the atezo-only arm.

As a result, the patients receiving TIGIT PD-L1 combination received 30% less the -- antibody versus controller. So safety really impacted the ability to administrate treatment and, therefore, probably impacted the outcome. We've always advocated for the Fc-reduce formats, and we believe that the data starting to support our convention, not all anti-TIGIT antibodies are the same. And we believe the market is missing this. We believe our assets are positioned to capture the upside as new data emerges with readouts anticipated from 2026, provided our conviction proves correct.

This moves us to our strategy, which is rooted in science and focused on patients. We have 5 key value drivers, starting on Fc-reduced TIGIT programs. COM902 is one of the only 2 clinical stage Fc reduced antigenic monoclonal antibodies currently in clinical development. And importantly, it's fully owned by Compugen. Positive Phase III data from Arcus Gilead with the only other known Fc reduced anti-TIGIT monoclonal antibody is expected in 2026 and could be a real catalyst for COM902. Notably, recent overall survival data from their Phase II frontline gastric cancer study, which is the same setting as Arcus Gilead ongoing FET trial was presented at ESMO recently and showed a median Argo survival of 27 months versus 15 months or less for benchmarks, a meaningful signal for the Fc reduced class.

Next is Rifugostomix. Our partner, AstraZeneca Fc reduced anti-PD-1 TIGIT bispecific with the TIGIT component derived from RFC reduced high affinity COM902. Interestingly, cooperative bispecific binding might provide even further efficacy into PD-1 and TIGIT blockade, while in addition, potentially supporting an easier regulatory path. The potential commercial opportunity for real way substantial with AstraZeneca estimating nonrisk-adjusted peak year revenue target of more than $5 billion. We understand that AstraZeneca's ambition is for forever to replace PD-1 PD-L1 therapies and to service the backbone for future combination treatments.

Their broad development program spanning 11 Phase III trials across lung, gastrointestinal and endometrial cancers represent a potential significant value driver for Compugen as we're eligible for regulatory and commercial milestones and mid-single digit tiered royalties payments. Moving to Fc-reduced PVRIG, COM701, fully owned and the only Fc-reduced monocolonal -- antibody in the clinic, which again, we believe is the right Fc-format. The biology here is truly differentiated from PD-1 and TIGIT checkpoints, providing advantages that we believe could translate into clinical benefit for patients with platinum-sensitive ovarian cancer.

Positive data in our ongoing MIOviral platform trial could support a product like development program aimed at addressing a significant unmet medical need. And finally, to our KulanSmalt potential first-in-class antibody program, adversing cytokine biology, GS-0321 previously COM503 is a potential first-in-class anti-icinbinding protein antibody licensed to Gilead. GS-0321 represents a novel antibody approach to harness -- biology for the treatment of cancer, potentially overcoming the limitations presented by illustration of therapeutic cytokines. It represents another potential value driver for Compugen, as we're eligible to receive $758 million in milestone payments and single-digit to low double-digit tiered royalties. This program is the most recent example of how our AI/ML power discovery engine is delivering new opportunities.

And behind this, we have early pipeline of what we believe to be truly innovative research programs. As pioneers in the field, we are committed to delivering real breakthroughs, not just incremental therapies. And really innovation is never easy. It takes time, persistence and willingness to tackle the toughest scientific challenges. But I believe deeply in what we're doing here, and we have the best talent and great tools to do this and are truly excited about the potential of our early stage programs.

Next, turning to the progress we have made this quarter. The team at ESMO in Berlin in October represented the full analysis of our 3 previously reported Phase I trials, reflecting the clinical benefit of COM701 as monotherapy and in combination in patients with heavily pretreated platinum-resistant ovarian cancer. The pooled analysis demonstrated that COM701 was well tolerated, showed consistent durable responses in patients with heavily pretreated platinum-resistant ovarian cancer, particularly in those without liver metastasis, representing patients with lower disease burden and potentially less immunosuppressive tumor macroenvironment. The results of the analysis support the rationale for the ongoing randomized myoviral platform trial, evaluating COM71 its maintenance therapy in early lines of treatment.

The Myoviral platform trial is progressing -- sites have been activated across the U.S., Israel and France including major academical centers and multiple sites from the French oncology cooperative group, AkaciGenico, renowned for several recent platinum-sensitive ovarian cancer trials. We now estimate the interim analysis in Q1 2027. We believe Myovian is a significant opportunity to address an unmet need for maintenance therapy in platinum-sensitive ovarian cancer. Next, our partner, AstraZeneca, which presented new real bad data at ESMO as part of 2 mini-oral sessions. AutoMD 1 follow-up shows that river was well tolerated with promising efficacy, confirming its potential in checkpoint-naive non-small cell lung cancer.

Notably, the drug-related discontinuation rate of only 3% further support differentiation of dept-reduced formats. The Tropin pan tumor 3 evaluating combination with -- showed promising efficacy and manageable safety underscoring the potential of next-generation IO bispecific plus ABC. Moving next to GS-0321, our novel antibody approach with Gilead that leverages cytokine biology, the Phase I trial is progressing as planned and represented a trial design at CIT last week. We have strong conviction in our fully owned programs. We are validating partnerships with AstraZeneca and Gilead providing potential for over $1 billion in milestones plus royalties.

Of course, none of this would be possible without our highly committed talented team here at Compugen who continuously performs at the highest level of excellence. With that, I will hand over to David for the financial update before we open up the floor for Q&A.

Thanks, Eran. I'm pleased to say that we are advancing in 2025 with a solid balance sheet. Cash runway, assuming no further cash inflows is expected to fund our operating plan into the third quarter of 2017 and we anticipate using this runway to advance our COM701 platinum-sensitive ovarian cancer trial, myaovarian and to support the progression of ZS-0321 in the clinic, together with continued investment in our early-stage pipeline. Going into the details, I will start with our cash balance. As of September 30, 2025, we had approximately $86 million in cash, cash equivalents, short-term bank deposits and investments in marketable securities. In October 2025, subsequent to the financial results for the quarter ended September 30, 2025, a total of approximately 0.8 million shares were sold through the company's ATM facility, contributing to a net proceeds of approximately $1.6 million.

Revenues for the third quarter of 2025 were approximately $1.9 million compared to approximately $17.1 million revenue for the comparable period in 2024. The revenues for the third quarters of 2025 and 2024 reflect the recognition of respective portions of both the upfront payment and the IND milestone payment from the license agreement with Gilead. Expenses for the third quarter of 2025 were in line with our plans. R&D expenses for the third quarter of 2025 were approximately $5.8 million compared to approximately $6.3 million in the third quarter of 2024. Our G&A expenses for the third quarter of 2025 were approximately $2.2 million and approximately $2.6 million for the same period in 2024.

For the third quarter of 2025, our net loss was approximately $6.98 million or $0.07 per basic and diluted share compared to a net profit of approximately $1.28 million or $0.01 per basic and diluted share in the third quarter of 2024. With that, I will hand over to the operator to open the call for questions.

[Operator Instructions] The first question is from Stephen Willey of Stifel.

Just curious, the extension of the Maya interim analysis from, I guess, the second half of 2016 into the first quarter of 2017. Is that just predicated on enrollment time lines and kind of what you're seeing just from an accrual perspective. Does that have anything to do with the accumulation of PFS events in the study that may be required to trigger the interim, just curious as to what's kind of happening behind the scenes there?

Sure. Thanks, Steve. So overall, as we know, there are a few factors that determine the initial readouts of clinical trials. This opening the sites is the actual enrollment rates. And finally, the actual accumulation of events along the trial. And we saw the -- estimation and the more the trial develops, you understand the kinetics and you optimize your prediction, and this is exactly what we're doing here. We can say today that we opened most of the sites, including major academical U.S. centers and the French Clinical Group. It took a bit more time to open it's mostly academical centers, but we are glad to have them on board. And now again, most of them are open.

And now we expect while opening the sites, and again, and heading the French site also was done because they showed interest and also to support the aggressive enrollment trade that we anticipate. And now this is the time for the start enrollment and see the actual ramp-up. And Michelle, if you want to add something to add some color?

No. I mean, you covered everything. So effectively, we had selected a number of sites. We've had additional academic sites wanting to participate. And those do tend to take a little longer to open. In addition to that, we had also been consulting with Geneco in France when they asked to participate as well. So we're trying to reflect our best estimates. I think there's a lot of different factors that impact when 1 has an interim analysis, and we still believe that we will be able to meet the aggressive time lines that we have.

And finally, we also disclosed today that we have cash runway into Q3 '27. So we also have the cash to support taking into account this shift in Q1. So through an good position to continue with the trial and to bring value profession because we think -- we believe in this study. .

The next question is from Daina Graybosch of Leerink Partners. Please go ahead.

I wonder if we could talk about the upcoming ARCUS Gilead readout with -- and gastric cancer because it could come as early next year. What do you know what you're looking for, of course, if it's successful, then that validates your ingoing hypothesis. But is there anything you would see in the outcomes of that trial that would reduce your confidence in your own TIGIT and more importantly, in the bispecific Rovigo.

Thank you, Daina. It's a very good question. So this will be the first Phase III readout for a reduced digit antibody. The data enabled is promising, but it was a single-arm study, not many patients, but doubling -- almost doubling the overall survival versus -- control was reassuring. And now is the time to see how it evolves in the Phase III, and this is, of course, could be very meaningful for us. But it is only 1 trial. So obviously, if it's successful, this reflects directly on the Fc-reduced and what we're saying about the Fc-active the safety issues, potential reduced efficacy issues, and this will show directly that Fc reduced are active in Phase III results. But even if this trial fails, ARPU deal themselves as additional Phase II Phase III trials, additional 2 ones. And AstraZeneca has 2 additional advantages over the -- just a single monoclonal Fc-reduced. One is they show that they're bispecific has a potential more activity. And actually, it shows up in a very nice ex vivo patient-derived material system, and they have a cooperative binding that allow cooperative blockade of PD-1 and TIGIT on the same cell.

And the result was in that relatively trastational system that is more active than just PG1- TIGIT blockade. And then also in some of the trials, that a potential regulatory advantage is the way we see it and looking just for the size of all the accumulating Phase III trials, for example, run of the the trials in the -- I believe the -- BLRA01 that comparing real plus chemo to -- and because it's a bispecific, nobody can ask for a contribution of components as far as we understand it. And therefore, you don't need to show that TIGIT is active. Yes, we believe TIGIT is active, and they have to reduce. But even if the activity is not sufficient in this case, having both enhanced efficacy due to the bispecific format and just using it -- as a safe backbone to combine with chemo to compare versus chemo. This is definitely an advantage of the bispecific. There are some other trials doing the same. And they also have some trials doing directly head-to-head versus pembro.

And we believe and think that they should have a win there as well. But so they have multiple shots on goal with some advantages of the bispecific in this.

The next question is from Lena Gershell of Oppenheimer.

Just wondering if you -- as we look forward to the interim update from my ovarian, could you remind us of any internal threshold or bar you're looking for from that interim with respect to efficacy.

Thank you, Leland. So I will turn the hand over to Michelle so again, just to remind everyone, we talked about a study which have 40 patients treated with COM701 in maintenance settings compared to 20 patients in placebo. We're relying on solid -- control -- and internal control compared to placebo. This is not a registration trial, but we are looking, and we think this trial is built to allow us to understand if COM701 has a monotherapy signal in this patient population after seeing a signal in the last-line lung resistance setting. And then upon success, this adaptive trial design will allow us to build and to continue to move forward either to adding more arms or to potential -- approval. And Michelle, please add some color on that.

Okay. So the clinical trial is an exploratory study to allow us to determine the magnitude of the effect size of COM701. It is very desirable for us to be able to demonstrate single agent activity, an improvement of up to 3 months above the placebo would be very clinically meaningful. But at the same time, we are looking forward to the totality of the data to be able to determine what the next best steps would be.

The next question is from Asthika Goonewardene of Truist Securities.

So with COM902, this would test to be an unpartnered actually reduced TIGIT antibody in the way new data coming up from the people who were watching on Arcus and making read-throughs here. So I know you've licensed to bind at your AstraZeneca, but does that still give you flexibility to partner in IoT with a separate company. Can you let us know about any restrictions or financial terms we should take into consideration?

Thanks, Asthika. It's a great question. So we licensed AstraZeneca, the rights to use COM902 as part of their bispecific PD-1 and TIGIT and some other bispecifics. But we fully own covenant. We don't have any restrictions. We can either decide to move forward in our own trials, obviously, upon successful results by others to be a meaningful driver, remind love that in the days that the active TIGIT initial deals were hundreds of millions of dollars of upfront deals and being the probably only monoclonal Fc-reduced-digit antibody other. We believe that redos in 26 could bring meaningful interest back into TIGIT, especially in COM902 and we have -- again, we fully own it. So it's we can be fully opportunistic in whatever direction we would like to take this COM902. .

The next question is from [indiscernible] H.C. Wainwright.

Good morning, Eran and David, thanks for taking questions. A couple of quick questions. One is when we you look at the tolerability profile of comps alone. How does that influence its potential use in combination therapies, especially in some of the less immune influent tumors. And the other question is, when you saw the data from the pooled analysis presented at ESMO. There were some great 3 or higher treatment-related adverse ones about 16.7% results. So how does -- how do you plan to include that safety in combination therapies. .

Sure. So firstly, the tolerability of COM701 as a monotherapy is extremely well tolerated. In fact, we didn't have any discontinuations due to adverse events in that pooled analysis when COM701 was used as a single agent. And in the triplet combination groups in the pooled analysis, the adverse events that we're seeing that were grade 3 were in keeping with the same frequency seen in respect of labels for both nivolumab and pembrolizumab. Given the tolerability of COM701, we believe that it is very well set up for being able to be used as a monotherapy or as a combination with standard of care agents or with other novel agents that are coming through the landscape.

This concludes the Q&A session in Compugen's investors conference call. Thank you for your participation. You may go ahead and disconnect.