Ladies and gentlemen, thank you for joining us today. Welcome to Compugen's First Quarter 2025 Results Conference Call. At this time, all participants are in listen-only mode. An audio webcast of this call is available in the Investor 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, Vice President, Head of Investor Relations and Corporate Communications. Yvonne, please go ahead.

Thank you, operator, and thank you all for joining us on the call today. Joining me from Compugen for the prepared remarks are Dr. Anat Cohen-Dayag, President and Chief Executive Officer; and David Silberman, Chief Financial Officer. Dr. Michelle Mahler, Chief Medical Officer, and Dr. Eran Ophir, Chief Scientific 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 their potential outcomes, the company's discovery platform, anticipated progress and plans, results and timelines for our programs, 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. And with that, I'll turn the call over to Anat.

Thank you, Yvonne, and a warm welcome to everyone joining our call today. To start, I would like to refer to the announcement we shared a few days ago regarding key leadership transitions at Compugen. After 15 years as President and CEO of the company, I am very happy to be assuming the newly created position of Executive Chair and to be handing the reins over to the very capable hands of Eran Ophir. Over the past years, we have accomplished a lot, including advancing our innovative clinical immunotherapy pipeline, establishing strategic collaborations, building a robust foundation with a talented management team, and ensuring a cash runway into 2027. This is the right moment to pass the leadership to Eran, who has been my trusted partner and Compugen’s Scientific leader for the past five years. We believe this combination of leadership ensures a solid foundation for the company's next phase of growth. I would also like to thank Paul Sekhri, who after eight years will step down as Chair of the Board. Paul has been a great mentor to me and contributed significantly to the success we have achieved at Compugen. On the call today, I will provide an update on progress we have made this quarter in our mission to transform the lives of cancer patients. In the first quarter of 2025, we continue to advance our early-stage and clinical immuno-oncology pipeline. Starting with our potential first-in-class anti-PVRIG antibody COM701, we initiated the first sub-trial of our adaptive platform trial comparing COM701 maintenance therapy to placebo in 60 patients with relapsed platinum-sensitive ovarian cancer. The patients progressing post-PARP inhibitors and/or bevacizumab or who are not candidates for such treatment represent an area of unmet medical need with no treatment option. Our study focuses on helping these women. With the support of our investigators, we're engaged with the site activation and are working diligently to proceed with dosing the first patient. We intend to share interim analysis from this sub-trial in the second half of 2026. The clinical trial landscape is evolving following the success of ADC in platinum-resistant ovarian cancer. And ADCs are also being evaluated now earlier in the disease course in patients with platinum-sensitive ovarian cancer, as replacements to chemotherapy and added to chemotherapy. We believe that advancing COM701 in the maintenance setting of platinum-sensitive ovarian cancer is where COM701 may present its potential advantages in terms of tolerability and durability. As previously communicated, we believe that showing a three-month improvement over the median progression-free survival of the placebo would be clinically meaningful. Positive data has the potential to serve as a key catalyst in advancing a broader clinical development program to address significant unmet medical needs. Moving next to the TIGIT landscape. Despite failures in the TIGIT space, it is notable that companies with Fc-inactive anti-TIGIT, like AstraZeneca and Arcus Gilead, are advancing their program. We have consistently advocated that Fc-inactive antibodies may serve as the better antibody format for targeting TIGIT. In line with this, current clinical trials suggest that Fc-inactive anti-TIGIT may have a safety advantage in certain patient populations, which could support a potential efficacy advantage due to patient durability on study treatment. With the multiple Phase 3 failures in TIGIT studies despite positive Phase 2 randomized studies, we believe that only a success in one of the upcoming Phase 3 trials could validate the TIGIT antibodies as a drug class, change the market sentiment, and open new opportunities for us as one of the few companies that have an Fc-inactive clinical stage TIGIT antibody. Clinically, we continue to believe that TIGIT PD-1 blockade may need to be combined with a PVRIG inhibitor to expand their use to lessen inflamed PD-L1 low tumors. So positive TIGIT PD-1 data by others may present additional opportunities for us. In addition, our partner AstraZeneca has the largest ongoing Phase 3 program in the TIGIT space. They have most recently initiated their 10th Phase 3 clinical trial with rilvegostomig, their PD-1 TIGIT bispecific, the TIGIT component of which is derived from our COM902. Since our last report in March 2025, AstraZeneca has initiated three additional Phase 3 trials in lung, gastric, and now also in a new tumor type endometrial. These new trials are evaluating rilvegostomig as monotherapy and combination therapy. The potential commercial opportunity for rilvegostomig is substantial, with AstraZeneca estimating non-risk adjusted peak year revenue targets of more than $5 billion. In lung cancer alone, the eligible lung cancer patient population across G7, based on 2025 EpiData, is estimated by AstraZeneca to be over 0.5 million patients. AstraZeneca's broad development strategy for rilvegostomig to replace existing PD-1 and PD-L1 inhibitors represents a significant potential revenue source for us, as we're eligible for both future milestone payments and mid-single-digit royalties on future sales. Coming up at ASCO 2025, AstraZeneca plans to present as a poster the first rilvegostomig ADC combination data from the Phase 3 TROPION-Lung04 trial evaluating frontline rilvegostomig in combination with Dato-DXd in non-small cell lung cancer. AstraZeneca also plans to present a poster with the first data from the Phase 2 GEMINI-Hepatobiliary trial evaluating frontline with rilvegostomig in combination with chemotherapy in treatment-naive biliary tract cancer. Moving next to GS-0321, formerly known as COM503, a potential first-in-class anti-IL18BP antibody licensed to Gilead. GS-0321 represents a novel way to harness IL-18 pathway biology for the treatment of cancer, potentially avoiding the challenges presented by administration of therapeutic cytokines. The Phase 1 trial is progressing as planned. Finally, beyond our clinical stage program, our teams are committed to progressing our extensive, innovative, and differentiated early-stage pipeline focused on potential first-in-class drugs and novel mechanisms of action aiming to address various mechanisms to enhance anticancer immunity. With a diverse pipeline and strong focus on execution in 2025, we believe Compugen is well positioned for growth. Test runway assuming no further cash inflow is expected to fund our operating plans into 2027, and we anticipate using this runway to advance our COM701 platinum-sensitive ovarian cancer trial and to support the progression of GS-0321 in the clinic together with continued investment in our early-stage research pipeline. Of course, none of this would be possible without our highly committed talented team here at Compugen, who continuously perform at the highest levels of excellence. I'm excited for 2025 to be another year of advancing our efforts to make a meaningful impact on cancer patient lives. With that, I will hand over to David for the financial update before we open the floor for Q&A.

Thank you, Anat. I am delighted to say that we are advancing into 2025 with a solid balance sheet, with no debt and with a cash runway to support our operating plans into 2027. Our cash runway takes into account the planned development of our clinical assets and continued investment in our early innovative pipeline and does not include any additional potential cash inflows. Going into the details, I will start with our cash balance. As of March 31, 2025, we had approximately $103.7 million in cash, cash equivalents, short-term bank deposits, and investments in marketable securities. Revenues for the first quarter of 2025 were approximately $2.3 million compared to approximately $2.6 million of revenue for the comparable period in 2024. The revenues in the first quarter of 2025 reflect the recognition of portions of both the upfront payment and the IND milestone payment from the license agreement with Gilead, while in the first quarter of 2024 that reflects portions of the upfront payment from the license agreement with Gilead. Expenses for the first quarter of 2025 were in line with our plan. R&D expenses for the first quarter of 2025 were approximately $5.8 million compared to approximately $6.4 million in the first quarter of 2024. Our G&A expenses for both the first quarter of 2025 and 2024 were approximately $2.4 million. For the first quarter of 2025, our net loss was approximately $7.2 million or $0.08 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 first quarter of 2024. With that, I will hand over to the operator to open the call for questions.

Thank you. Ladies and gentlemen, we will now start the question-and-answer session. The first question is from Daina Graybosch from Leerink Partners.

Hey, Anat. I have two questions regarding the competitive landscape. Merck recently announced that their Phase 3 trial KEYNOTE-B96, which studies pembrolizumab in platinum-resistant ovarian cancer, was successful in improving overall survival in patients with PD-L1 expressing tumors. Could you discuss that success and its potential impact on your strategy in ovarian cancer if pembrolizumab is launched in that setting? I also have a follow-up.

Michelle, would you like to refer to this?

Sure. I'd be happy to refer to it. Thanks for the question, Daina. Yes. So this study is in platinum-resistant ovarian cancer. It's in third-line. So, it is in an earlier stage setting of patients in the disease process, whereas our studies are in platinum-sensitive, but we're also looking at second and third-line patients. So, I'm quite encouraged by their announcement because it means that there is benefit being seen by adding an immune checkpoint inhibitor to standard-of-care agents. And in the event that our study demonstrates activity, it opens up additional opportunities to be able to combine our COM701 in these settings and also, help drive taking it further to a broader population.

Great. And then I wonder, you talked about TIGIT and Fc competent or incompetent. I wonder if you could talk about your interpretation of Roche's SKYSCRAPER-01 data. What about the data specifically gives you confidence that the failure of that TIGIT was due to its Fc competency and not simply that TIGIT antagonism adds incremental clinical benefit?

Yes. Okay. So I'm going to make, you're going to take it, Eran. Okay. Go ahead. No, I'd go after you.

Sure. What we observe from the TIGIT trial with the Fc-active is that despite complications and high discontinuation rates, there is still some activity noted. We do see numerical activity. However, this study involved a patient population that had higher rates of brain metastasis compared to previous trials and CT scans. The statistical plan may have posed some challenges, along with the patient numbers. It's important to note that TIGIT blockade does not completely eradicate tumors, although it is still active. The presence of an active Fc combined with high discontinuation rates is significant. Companies like ours, AstraZeneca, and Arcus have not demonstrated activity in this area. The right patient population is crucial for the typical study design. Therefore, it is encouraging to see the activity of TIGITs that we need to complement PD-1 treatments, as there is numerical evidence of longer overall survival, prolonged progression-free survival, and higher overall response rates. The results in this study, given its size and the patient population despite high discontinuation rates, were adequate to suggest that TIGIT could lead to approval. We are looking forward to the outcomes of upcoming trials involving Fc-non-active TIGITs.

Yeah. So I'm going to agree with what Eran said, and I think that there are definite nuggets in terms of the type of patients between the CITYSCAPE study and the SKYSCRAPER study. And I think the populations were not the same. So the activity seen in the one study did not translate into the second study. So I think there's still more to be learned. And again, I think that the discontinuation rate in SKYSCRAPER-01, as well as the number of patients with metastases to the brain and liver probably also impacted their data and outcomes.

I'll add that the safety and tolerability of the Fc disabled may affect not only the discontinuation and efficacy of these assets but also their potential for combination with other therapies. The upcoming studies testing combinations with chemotherapy and ADCs could be very significant. I believe that only Phase 3 data will provide clarity in this area. We have substantial Phase 2 data indicating that adding TIGIT to PD-1 is valuable, but the real impact will come from strong Phase 3 results. I hope that with positive data from the Fc disabled, starting with Arcus and then AstraZeneca after 2026, we can shift the sentiment positively.

Great. Thank you, guys.

The next question is from Rohan Mathur of Oppenheimer. Please go ahead.

Hi. Thanks for taking the question. This is Rohan on for Leland Gershell. Just a couple from me. One was, do you plan to collect data on the tumor microenvironment features from the 701 study, like, PVR expression or IFN signatures? And the other would be, as you think about the maintenance setting for platinum-resistant patients, what would you like to see from a clinically meaningful perspective on PFS benefit? Thank you.

So to answer your first question, we will definitely be collecting data to be able to evaluate the tumor microenvironment. We do have a biomarker plan, but I'm not going to comment further on the details since it's not in the public domain. And regarding the maintenance setting, so in platinum-sensitive, which is where our maintenance study is taking place. We do know from multiple Phase 3 benchmark studies, both bevacizumab as well as for the PARP inhibitors, the progression-free survival in patients on all of those placebo arms, whether they were in second-line treatment or third-line treatment, tended to range between 5.4 months and 5.8 months. There was one outlier of 3.8 months, which has to do with the baseline genetic makeup of the patient population. So, we feel that an improvement that exceeds around three months would be clinically meaningful.

Great. Thank you.

The next question is from Asthika Goonewardene of Truist. Please go ahead.

Good morning, everyone. Thank you for taking my question. I want to follow up on Daina's inquiry regarding B96. Can you clarify whether 701 is effective with it and if you've observed any activity in PD-L1 positive patients? I'm aware of the increases in the platinum-resistant setting, but I'm curious if you have any insights on that and how it might influence potential combinability if PD-1 receives approval in late-line treatment. Additionally, there's a lot of current interest in PD-1 VEGF bispecifics, and I have several questions for you on that, Anat. First, have you explored the impact of adding VEGF to TIGIT plus PD-1? Can you share any observed synergies? Does the Fc inactive strategy apply in this context as well? And have you shared any of this data with your partners at Fc? Thank you.

So I will take some of your questions and then defer to Eran for further input. So to start with the question about activity in patients who are PD-L1 positive or negative. In our platinum-resistant data, we have presented in the past that we see activity both in PD-L1 positive and negative patients. And it's one of the reasons why we believe that when we use COM701, it tends to be a PVRIG-mediated activity because traditionally single-agent PD-1 inhibition in platinum-resistant patients has not been very effective. As far as the PD-1 VEGF, I'm going to have Eran comment.

Thank you, Michelle, and thank you, Asthika, for the question. So just to add a bit about the PD-L1. What is really interesting and what we have shown quite extensively is that PVRIG biology is very different from PD-1, from TIGIT, and other checkpoints. And that is the reason why we think that we see this unique activity in places where checkpoints are typically not working, including in PD-L1 negative patients. We have a monotherapy activity of COM701 alone in a patient with a PD-1 negative tumor microenvironment. So definitely, we think that this will explain why PVRIG could be active. And now when we have some signal of activity of PD-1 blockade in the last line in combination with chemotherapy, we definitely think that it could be that when COM701 would be combined with PD-1, we can now treat also patients with PD-1 negative tumors that would not respond probably to PD-1 alone. About the PD-1 VEGF. So VEGF in general has a mechanism in addition to the anti-angiogenic effect to increase this infiltration. So from a mechanistic point of view, this could definitely go along with the biology of PVRIG blockade that increases this infiltration with other mechanisms. We do not publish any data on this regard. But we definitely could be a mechanism that would complement specifically PVRIG biology in addition to the other activities of any other checkpoints. And I don't think specifically that Fc active or non-active will matter mechanistically, but since the Fc active have, again, some safety challenges. And since it's yet to be seen if the PD-1 VEGF bispecific indeed really solves the side effects, combining what could be still some toxic agents like PD-1 VEGF with another somewhat toxic agent like Fc active TIGIT could be challenging. So we think that it will be preferable to combine these agents, including PD-1 VEGF with Fc non-active TIGITs.

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