Compugen Ltd.

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 Investors section of Compugen's website, .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. Anak Cohen-Diag, President and Chief Executive Officer, and David Sibberman, Chief Financial Officer. Dr. Michelle Malheur, Chief Medical Officer, and Dr. Ivana Burr, 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 of 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 filing for more details on these risks, including the company's most recent annual report on Form 20F. 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 Yvonne.

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 Ahran Ofeer. 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 teams, and ensuring a cash runway into 2027. This is the right moment to pass the leadership to Ahran, who has been my trusted partner and competent 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 Secre, 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 immunoncology pipeline, Starting with our potential -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-op inhibitors and or bevacizumab, or who are not candidates for such treatment, represent an area of unmet medical needs with no treatment options. Our study focuses on helping these women. With the support of our investigators, we are engaged with the site activation and are working diligently to perceive 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 ADCs 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 a significant unmet medical need. Moving next to the TGIT landscape. Despite failures in the TGIT space, it is notable that companies with FCE-inactive anti-TGIT like AstraZeneca and Arcus Gilead are advancing their program. We have consistently advocated that FCE-inactive antibodies may serve as the better antibody format for targeting TGIT. In line with this, current clinical trials suggest that FCE-inactive anti-TGIT 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 III failures in TGIT studies, despite positive Phase II randomized studies, we believe that only a success in one of the upcoming Phase III trials could validate the TGIT antibodies as a drug class, change the market sentiment, and open new opportunities for us as one of the few companies that have an FCE-inactive clinical stage TGIT antibody. Clinically, we continue to believe that TGIT PD-1 blockades may need to be combined with a PBRID inhibitor to expand their use to less inflamed PD-L1 low tumor. So positive TGIT PD-1 data by others may present additional opportunities for us. In addition, our partner AstraZeneca has the largest ongoing Phase III program in the TGIT space. They have most recently initiated their 10th Phase III clinical trial with Rizagosto to make their PD-1 TGIT by specific, the TGIT component of which is derived from our Comp902. Since our last report in March 2025, AstraZeneca has initiated three additional Phase III trials in lung, gastric, and now also in a new tumor type, endometrial. These new trials are evaluating Rizagostomy gizmonotherapy and combination therapy. The potential commercial opportunity for Rizagostomy is substantial, with AstraZeneca estimating non-risk adjusted PQ revenue targets of more than $5 billion. In lung cancer alone, the eligible lung cancer patient population across G7, based on 2025's epi data, is estimated by AstraZeneca to be over half a million patients. AstraZeneca's broad development strategy for Rizagostomy to replace existing PD-1 PD-L1 inhibitors represents a significant potential revenue source for us, as we're eligible for both future months on payments and meet single-digit tiered royalties on future sales. Coming up at ASCO 2025, AstraZeneca plans to present as a poster the first Rizagostomy ABC combination data from the Phase II tropion lung O4 trial, evaluating frontline Rizagostomy in combination with DatoDXB in also cell and cancer. AstraZeneca also plans to present a poster with the first data from the Phase II Gemini hepatobiliary trial, evaluating frontline Rizagostomy in combination with chemotherapy in treatment naïve biliary tract cancer. Moving next to GS0321, formerly known as COMPFY for free, a potential -in-class anti-RL18 binding protein antibody licensed to Gilead. GS0321 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 I trial is progressing as planned. Finally, beyond our clinical stage program, our teams are committed to progressing our extensive, innovative, and differentiated early stage pipelines focused on potential -in-class drugs and novel mechanisms of action, aiming to address various mechanisms to enhance anti-cancer immunity. With a diverse pipeline and strong focus on execution in 2025, we believe COMPGEN is well positioned for growth. This runway, assuming no further cash inflow, is expected to fund our operating plans into 2027, and we anticipate using this runway to advance our COMP71 platinum-sensitive ovarian cancer trial and to support the progression of GS0321 in the clinic, together with continuing investment in our early stage research pipeline. Of course, none of this would be possible without our highly committed, talented team here at COMPGEN, 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 patients' lives. With that, I will hand over to David for the financial update before we open the floor for Q&A.

Thank you, Annette. I am delighted to say that we are advancing in 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 plan 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, total bank deposits, and investment 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 -of-term payment from the license agreement with Gilead, while in the first quarter of 2024 they reflect 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 GNE 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. If you have a question, please press star 1. If you wish to decline from the polling process, please press star 2. If you are using speaker equipment, kindly lift the handset before pressing the numbers. Please stand by while we poll for your questions. The first question is from Dana Gryowich from Lerink Partners. Dana,

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, you know, pembrolizumab, we haven't seen the results, if they ultimately launch pembrolizumab in that setting, your strategy in ovarian cancer. And then I have a follow-up.

Michelle, would you like to refer

to this? Sure. Sure, I'd be happy to refer to it. Thanks for the question, Dana. Yeah, 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 study is 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 audience.

Great. And then I wonder, you know, we talked about TIDGET and FC-competent or incompetent. I wonder if you could talk about your interpretation of Roche's skyscraper one data. What about the data specifically gives you confidence that the failure of that TIDGET was due to its FC competency and not simply that TIDGET and competent data? Yes, I think that the TIDGET antagonism adds incremental clinical benefit. Yes.

Okay, so I'm going to make... Oh, you're going to take it, Aaron. Okay, go ahead. No, I'll go after you.

Sure. So, yeah, what we see is I think what we tend to see from this TIDGET trial with the FC active. We see that even in this trial, even all the complication of the FC active and high disconsideration 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-SCA for example, the statistical plan maybe was a bit challenging, maybe also the number of patients. So I think, no, we know that TIDGET in contrast to mice, TIDGET 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 and you have high discontinuation rate, it matters. As a reminder, ourselves, AstraZeneca, Argus have a non-active FC. And then also if the right patient population is critically important, the statistical design, so I think what you're encouraged to see, again, is definitely an activity of TIDGETs that when it's added to PD-1, we see numerically that there is longer over survival, longer OPFS, higher ORR. It was not sufficient in this study, in this size, in this patient population, and with the high discontinuation rates typical to -ACTIV-TIDGET to lead to approval. And we definitely are eager to see how the coming trials with -ACTIV-TIDGETs will turn out. Michelle?

Yes. Yes, so I agree with what Erin 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 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 1, as well as the number of patients with metastasis to the brain and liver, probably also impacted their data and outcomes.

And

I'll

add just one more thing that I think, you know, that the safety or the tolerability of the FC disabled may also turn these assets, 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 three data will make a difference in this field. And I think that we have a lot of phase two data that are showing in randomized studies that are showing that the TGIT addition to PD-1 adds value. And I think that the only thing that will matter is to see very good phase three data. Hopefully with the FC disabled, either from ARCUS first and then from AstraZeneca Beyond 26, only positive data will change the sentiment, I believe.

Great.

Thank

you, guys. The next question is from Rohan Masur of Oppenheimer. Please go ahead.

Hi, thanks for taking the question. This is Rohan for leaving their show. Just a couple from me. One was, do you plan to collect data on the tumor microenvironment features from the 701 study like PBR expression or IFM 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 three benchmark studies, both for Bevacizumab as well as for the POP 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 had 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 Asitika Gunnawardene of Truist. Please go ahead.

Hi guys, good morning. Thanks for taking my questions. Just want to tag on to Dana's question about B96. Can you remind us, does 701 work with that? Have you seen specifically activity in PD-01 positive patients? Just wondering if, I know B96 is in the platinum resistant setting, but I'm just wondering if you have seen that and maybe you can make some read-throughs into what the combinability would look like in the event that PD-01 gets approved in the late-line setting too. Secondly, PD-01 VEGF by specific is a lot of interest these days. I have a multi-part question for you on that. One, have you looked at what adding VEGF does to TGIT plus PD-01? And can you talk about any synergy that you've observed? Does the FC inactive strategy make sense here too? And have you discussed any of this data with your partners at AZ? 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 that are PD-01, whether they're positive or negative. So in our platinum resistant data we have presented in the past that we see activity both in PD-01 positive and negative patients. And it's one of the reasons why we believe that when we use COM 701 it tends to be a PBRG mediated activity because traditionally single agent PD-01 inhibition in platinum resistant patients has not been very effective. As far as the PD-01 VEGF, I'm going to have Eran comment.

Yeah, thank you, Michelle, and thank you, Azjika, for the question. So just to add a bit about the PD-01. So what is really interesting and what we have shown quite extensively that PBRG biology is very different from PD-01, from TGIT 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-01 negative patients. We can have a monotherapy activity of COM 701 alone in a patient with a PD-01 negative 2-MI environment. So definitely we think that this will explain why PBRG could be active. And now when we have some signal of activity of PD-01 blockade in the last line in combination with chemo, we definitely think that it could be that when COM 701 would be added potentially also to PD-01, we can now treat also patients with PD-01 negative that would not respond properly to go to PD-01 alone. About the PD-01 VHF. So VHF in general has a mechanism in addition to the anti-adrogenic effect to increase tissue infiltration. So mechanistically, point of view, this could definitely go along with the biology of PBRG blockade that increased tissue infiltration with other mechanisms. We didn't publish any data on this regard, but we definitely could be a mechanism that would complement specifically PBRG biology in addition to the other activities it's 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-01 VHF by specific indeed really solves the BEV side effects. So the combination of what could be still some toxic agent like PD-01 VHF with another toxic agent like FC active could be challenging. So I think that here as well, it would be preferable to combine any kind of this agent including PD-01 VHF with an FC non-active digit.

This concludes the Q&A session and Compugens Investor Conference call. Thank you for your participation. You may go ahead and disconnect.