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 outcome, 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 few days ago regarding key leadership transitions at Compugen. After 15 years as President and CEO of the company, I'm 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 collaboration, building a robust foundation with 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…

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, at this time, we will begin the question-and-answer session. [Operator Instructions] First question is from Daina Graybosch from Leerink Partners.

Hey, Anat. Two questions for me more on the competitive landscape. Merck recently announced that KEYNOTE-B96, which is a trial Phase 3 studying pembrolizumab and platinum resistant ovarian cancer was successful and hit on overall survival in patients that have tumors that express PD-L1. I wonder, if you could talk about that success, and how that could impact if Pembro -- we haven't seen the results, if they ultimately launch Pembro in that setting, your strategy in ovarian cancer? And then, I 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 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. So, yeah, what we see is, I think what we tend to see from this TIGIT trial with the Fc active. We see that even in this trial, even though the complication of the Fc-active and high discontinuation rates, we still see activity. We definitely see numerical activity. But overall, in this study, in the patient population that they chose also they had higher rates of brain metastasis in this patient compared to previous trials and CT scan, for example. The statistical plan maybe was a bit challenging, maybe also the number of patients. So I think we know the TIGITs in contrast to mice, TIGIT blockade is not causing to complete melting of all tumors, but we know it's active. And now this is matter -- so if you have an active Fc, we have high discontinuation rate, it matters. As a reminder, ourselves, AstraZeneca, Arcus have non-activity. And then also if the right patient population is critically important, it's typical design. So I think what you are encouraged to see, again, definitely an activity of TIGITs that we need added to PD-1, we see numerically that there is longer over survival, longer OPFS, higher ORR (ph). It was a sufficient in this study, in this size, in this patient population and with the high discontinuation rate typical to have set the TIGIT to lead to approval and we definitely are eager to see how the coming trials with Fc-non-active TIGITs will turn up. Michelle?

Yeah. So I'm going to agree with what Eran said, and I think that they 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 different -- sorry, we're 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.

And I'll add just one more thing that I think that the safety or the tolerability of the Fc disabled may also turn these assets not -- it may not only affect the discontinuation and then the efficacy, but it may also turn them to be more combinable. And I think that with the next studies that are being done, testing also combinations with chemo, combinations with ADCs that may be very relevant. And on this front, I think that only Phase 3 data will make a difference in this period. And I think that we have a lot of Phase 2 data that are showing in randomized studies that are showing that the TIGIT addition to PD-1 at value. And I think that the only thing that will matter is to see a very good Phase 3 data. Hopefully, with the Fc disabled either from Arcus first and then from AstraZeneca beyond ‘26, only positive data, we changed the sentiment, I believe.

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 the first -- 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 have 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.

Hey, guys. Good morning. Thanks for taking my question. Just want to tack on to Daina's question about B96. Can you remind us, does 701 work with that, have you seen specifically activity in PD-L1 positive patients? Just wondering if -- I know there have been an increases (ph) in the platinum resistant setting, but I just wondering if you had seen that and maybe we can make some read-throughs into what the combinability would look like in the event that gets the PD-1 approved in the setting in the late line setting, too. Secondly, PD-1 VEGF bispecifics, a lot of interest these days. I have a multipart question for you on that, Anat. One, have you looked at what adding VEGF does to TIGIT plus PD-1? And can you talk about any synergy that you've observed? Does the Fc inactive strategy makes sense here too? And have you discussed 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 at a PD-L1, whether they positive or negative. So 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 and platinum-resistant patients has not been very effective. As far as the PD-1 VEGF, I'm going to have Eran to comment.

Thank you, Michelle, and thank you, Asthika, for the question. So just to add a bit about the PD-L1. So what is really interesting and what we have shown quite extensively that PVRG 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 macroenvironment. So definitely, we think that this will explain why PVRG could be active. And now when we have some signal of activity of PD-1 blockade in the last line in combination with chemo, we definitely think that it could be that when COM701 would be added potential also to PD-1, we can now treat also patients with PD-1 negative, that would not respond probably to go to PD-1 alone. About the PD-1 VEGF. So VEGF in general has a mechanism in addition to the anti-radiogenic (ph) effect to increase this infiltration. So mechanistically point of view, this could definitely goes along with the biology of PVRIG blockade that increased this infiltration with other mechanism. 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 is doing with any other checkpoints. And I don't think specifically, the 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 bev side effects, so the combination of what could be still some toxic agents like PD-1 VEGF with another bit toxic agent like Fc active TIGIT could be challenging. So we think that here as well, it will be preferable to combine any kind of these agents, including PD-1 VEGF with an 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.