BitMine stock falls after CEO change and board appointments
Compugen Ltd reported its third-quarter 2025 earnings, revealing a revenue miss that contrasted with its earnings per share (EPS) expectations. The company met EPS forecasts, posting a loss of 0.07 USD per share, consistent with analyst predictions. However, revenue fell short, coming in at 1.9 million USD against a forecast of 3.13 million USD, a shortfall of 39.62%. Despite the revenue miss, Compugen’s stock rose 3.7% in premarket trading, reflecting investor optimism about the company’s strategic partnerships and product pipeline.
Key Takeaways
- Compugen’s Q3 2025 EPS matched forecasts at -0.07 USD.
- Revenue significantly missed expectations, at 1.9 million USD.
- Stock rose 3.7% in premarket trading despite financial challenges.
- Strategic partnerships with AstraZeneca and Gilead remain a key focus.
- Cash runway is secure, extending into Q3 2027.
Company Performance
Compugen’s performance in Q3 2025 highlighted ongoing financial challenges with a net loss of 6.98 million USD. The company reported a significant decline in revenue compared to Q3 2024, where it achieved 17.1 million USD. However, the company’s focus on innovation in drug discovery and strategic partnerships with industry giants like AstraZeneca and Gilead is seen as a positive long-term strategy.
Financial Highlights
- Revenue: 1.9 million USD (down from 17.1 million USD YoY)
- Earnings per share: -0.07 USD (met forecast)
- Cash balance: 86 million USD as of September 30, 2025
- Raised 1.6 million USD through ATM facility in October 2025
Market Reaction
Despite the revenue miss, Compugen’s stock saw a 3.7% increase in premarket trading, reaching 1.68 USD. This positive movement could be attributed to investor confidence in the company’s strategic direction and product innovations, particularly in the cancer treatment space.
Outlook & Guidance
Compugen expects to continue its focus on computational drug target discovery and immune checkpoint inhibition. The company anticipates potential catalysts from ongoing trials and partnerships, including the Maya ovarian platform trial and potential milestone payments up to 1 billion USD.
Executive Commentary
CEO Eran Ophir emphasized the company’s pioneering role in computational drug target discovery, stating, "Real innovation is never easy. It takes time, persistence, and willingness to tackle the toughest scientific challenges." CFO David Silberman highlighted financial stability, noting, "Cash runway, assuming no further cash inflows, is expected to fund our operating plans into the third quarter of 2027."
Risks and Challenges
- Revenue decline may indicate market or operational challenges.
- Ongoing net losses could pressure financial resources.
- Dependence on milestone payments from partnerships for future growth.
- Potential delays in trial results or regulatory approvals.
- Competitive pressures in the biotechnology sector.
Q&A
During the earnings call, analysts inquired about the timeline extension for the Maya trial and the flexibility within the COM902 partnership. The management addressed these concerns, emphasizing the strategic importance of these initiatives and the positive tolerability profile of COM701 in various settings.
Full transcript - Compugen Ltd (CGEN) Q3 2025:
Conference Operator: Ladies and gentlemen, thank you for joining us today. Welcome to the Compugen Third Quarter 2025 Results Conference Call. At this time, all participants are in the 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, VP, Head of Investor Relations and Corporate Communications. Yvonne, please go ahead.
Yvonne Naughton, VP, Head of Investor Relations and Corporate Communications, Compugen: Thank you, Operator, and thanks everyone for joining us today. Here with me from the 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 their potential outcome. The company’s discovery platform, anticipated progress and plans, results, and timelines 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 and Form 20F. 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.
Eran Ophir, President and CEO, Compugen: 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 at such a pivotal time for our company. Having led our scientific strategy in my former position as CSO, I’ve seen firsthand how our science has evolved, and I believe we can deliver significant value for patients. 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 digital biology is now gaining clinical momentum. I think that now is a great time to highlight what makes us different in the digital 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-TIGIT 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 effector T cells and T regs, and this is not desired because, one, on efficacy, TIGIT is present on effector T cells, so similar to the action of anti-PD-1s, you want to reinvigorate these exhausted cells and avoid their depletion. Two, on safety, TIGIT is present on T regs. Depleting peripheral T regs could result in immune-mediated side effects.
FC-reduced anti-digits, like our own COM902, in contrast, preserve and reinvigorate effector T cells, avoid depletion of peripheral T regs, and therefore have the potential for improved immune activation and a better safety profile. It is notable that as early as phase two trials with FC-active anti-digits, safety was a concern with high rates of discontinuation due to adverse events. This was also even more evident in the phase three trials. For example, during recent ESMO meetings, the presenter highlighted that in SKYSCRAPER-07 trial, adding FC-active digit to atezolizumab resulted in these patients only receiving a median number of doses of 12 versus 17 in the atezolizumab-only arm. As a result, the patients receiving digit-PD-L1 combination received 30% less the PD-L1 antibody versus control. Safety really impacted the ability to administer treatment and therefore probably impacted outcome.
We’ve always advocated for the FC-reduced formats, and we believe that the data is starting to support our conviction. 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 readout 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 five key value drivers, starting on FC-reduced TIGIT programs. COM902 is one of the only two clinical-stage FC-reduced anti-TIGIT monoclonal antibodies currently in clinical development, and importantly, it’s fully owned by Compugen. Positive phase three data from domvanalimab, which is 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 two frontline grafted cancer study, which is the same setting as the Domvanalimab ongoing phase three trial, was presented at ESMO recently and showed a median overall survival of 27 months versus 15 months or less for benchmarks, a meaningful signal for the FC-reduced class. Next is Rilvegostomig, our partner AstraZeneca’s FC-reduced anti-PD-1 TIGIT bispecific with the TIGIT component derived from our FC-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 Rilva is substantial, with AstraZeneca estimating non-risk-adjusted peak year revenue target of more than $5 billion. We understand that AstraZeneca’s ambition is for Rilva to replace PD-1 and PD-L1 therapies and to serve as the backbone for future combination treatments.
Their broad development program, spanning 11 phase three trials across lung, gastrointestinal, and endometrial cancers, represents a potential significant value drive for Compugen as we’re eligible for regulatory and commercial milestones and meet single-digit tiered royalties payments. Moving to FC-reduced PVRIG, COM701, fully owned and the only FC-reduced monoclonal anti-PVRIG 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 Maya ovarian platform trial could support a broader clinical development program aimed at addressing a significant unmet medical need. Finally, to our GS0321 potential first-in-class antibody program addressing cytokine biology. GS0321, previously COM503, is a potential first-in-class anti-IL-18 binding protein antibody licensed to Gilead.
GS0321 represents a novel antibody approach to harness IL-18 pathway biology for the treatment of cancer, potentially overcoming the limitations presented by administration 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-powered discovery engine is delivering new opportunities. Behind this, we have early pipeline of what we believe to be truly innovative research programs. As pioneers in the field, we’re committed to delivering real breakthroughs, not just incremental therapies. Real innovation is never easy. It takes time, persistence, and willingness to tackle the toughest scientific challenges. I believe deeply in what we are doing here, and we have the best talent and great tools to do this.
I’m truly excited about the potential of our early-stage programs. Next, turning to the progress we have made this quarter, the team was at ESMO in Berlin in October, where we presented a pooled analysis of our three previously reported phase one 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 a potentially less immunosuppressive tumor microenvironment. The results of the analysis support the rationale for the ongoing randomized Maya ovarian platform trial evaluating COM701 as maintenance therapy in early lines of treatment. The Maya ovarian platform trial is progressing.
Sites have been activated across the US, Israel, and France, including major academic centers and multiple sites from the French oncology cooperative group Arcadia Gyneko, renowned for several recent platinum-sensitive ovarian cancer trials. We now estimate the interim analysis in Q1 2027. We believe Maya ovarian is a significant opportunity to address an unmet need for maintenance therapy in platinum-sensitive ovarian cancer. Next, our partner AstraZeneca, which presented new Rilva data at ESMO as part of two mini oral sessions. Our TOMAD-01 follow-up showed that Rilva was well tolerated, with promising efficacy confirming its potential in checkpoints naive non-small cell lung cancer. Notably, the drug-related discontinuation rate of only 3% further supports differentiation of the FC-reduced formats. The Tropion Pantumo-03, evaluating combination of Rilva with DataWay, showed promising efficacy and manageable safety, underscoring the potential of next-generation IO bispecific plus ADC.
Moving next to GS0321, our novel antibody approach with Gilead that leverages cytokine biology. The phase I trial is progressing as planned and represented last trial design at CT 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 milestone 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 the floor for Q&A. Thanks, Eran. I am 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 plans into the third quarter of 2027, and we anticipate using this runway to advance our COM701 platinum-sensitive ovarian cancer trial, Maya ovarian, and to support the progression of GS0321 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 investment 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 profit of approximately $1.6 million. Revenues for the third quarter of 2025 were approximately $1.9 million, compared to approximately $17.1 million of 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 R&D 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. 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 pooling process, please press Star 2. If you are using speaker equipment, kindly lift the handset before pressing the numbers. Please stand by while we pool for your questions. The first question is from Stefan Wiley of Stifel. Please go ahead. Yeah, good morning. Thanks for taking the question. Just curious, the extension of the Maya interim analysis from, I guess, the second half of 2026 into the first quarter of 2027, is that just predicated on enrollment timelines 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. Thanks. Sure. Thanks, Steve. Overall, as we know, there are a few factors that determine the initial readouts of clinical trials. It is opening the sites, it is the actual enrollment rates, and finally, the actual accumulation of events along the trial. We started trial-by-given estimation, and the more the trial develops, you understand the kinetics and you optimize your prediction. This is exactly what we are doing here. We can say today that we opened most of the sites, including major academical US centers and the French Arcadia Gyneco group. It took a bit more time to open, mostly the academical centers, but we are glad to have them on board. Now, again, most of them are open.
We expect while opening the sites, and again, adding the French sites also was done because they showed interest and also to support the aggressive enrollment rate that we anticipate. This is the time for the start enrollment and see the actual ramp-up. Michelle, if you want to add something to add some color? No, I mean, you covered everything. 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 bit longer to open. In addition to that, we had also been consulting with Gyneco in France when they asked to participate as well. We’re trying to reflect our best estimates.
I think there’s a lot of different factors that impact when one has an interim analysis, and we still believe that we will be able to meet the aggressive timelines that we have. Finally, we also disclosed today that we have cash run into Q3 2027. We also have the cash to support taking into account this shift in Q1. To remain in good position to continue with the Maya trial and to bring value for patients because we believe in this study. All right. Thanks for taking the question. The next question is from Diana Grey-Butch of Lyrion Partners. Please go ahead. Hi. Thank you for the question. I wonder if we could talk about the upcoming Arcus-Gilead readout with their TIGIT in gastric cancer because it could come as early next year. I want to know what you’re looking for.
Of course, if it’s successful, then that validates your ingoing hypotheses. 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 rilvegostomig? Thanks, Diana. It’s a very good question. This will be the first phase three readout for an FC-reduced TIGIT antibody. The data in it looked promising, but it was a single-arm study, not many patients, but doubling, almost doubling the overall survival versus historical control was reassuring. Now is the time to see how it evolves in the phase three, and this is, of course, could be very meaningful for us. It is only one trial.
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 three readouts. Even if this trial fails, Arcus Biosciences-Gilead themselves had additional phase two, phase three trials, additional two ones. AstraZeneca has two additional advantages over just a single monoclonal FC-reduced. One is they show that their bispecific has the potential for more activity, and actually showed it in a very nice ex vivo patient-derived material system, and they have a cooperative binding that allows cooperative blockade of PD-1 and PD-1 on the same cell. The result was in that relatively frustrational system that it’s more active than just PD-1 and PD-1 blockade.
Also, in some of the trials, they have a potential regulatory advantage as the way we see it, looking just for the side of all the accumulating phase three trials. For example, in one of the trials in the, I believe, the Artimide-Biliary-01, they’re comparing Rilva plus chemo to just chemo. Because it’s a bispecific, nobody can ask for a contribution of components as far as we understand it. Therefore, you don’t need to show that TIGIT is active. Yes, you believe TIGIT is active and the FC-reduced, but even if the activity is not sufficient, in this case, having both enhanced efficacy due to the bispecific formats and just using it as an IO safe backbone to combine with chemo to compare versus chemo, this is definitely an advantage of the bispecific.
They have 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. They have multiple shots on goal with some advantages of the bispecific indeed. The next question is from. The next question is from Leland Gershell of Oppenheimer. Please go ahead. Oh, hey, good morning. Thanks for the update and taking our question. Just wondering if you, as we look forward to the interim update from Maya ovarian, could you remind us of any internal threshold or bar you’re looking for from that interim with respect to efficacy? Thank you. Thank you, Leland. I will start to hand over to Michelle.
Again, just to remind everyone, we talk about a study which has 40 patients treated with COM701 in maintenance settings compared to 20 patients in placebo. We’re relying on solid historical control and internal control comparing to placebo. This is not a registration trial, but we are looking and we think this trial is well built to allow us to understand if COM701 has a monotherapy signal in this patient population after seeing a signal in the last line platinum-resistant setting. 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 accelerate approval. Michelle, please add some color on that. Okay. 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 three 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. Great. Thanks very much. The next question is from Astica Gudenwagen of Struis Securities. Please go ahead. Hey, guys. Good morning. Thanks for taking my question. With COM902, this would technically be an unpartnered FC-reduced TIGIT antibody in the wake of new data coming up from the people we are watching on Arcus and making read-throughs here. I know you have licensed the binder to AstraZeneca, but does that still give you flexibility to partner 902 with a separate company?
Can you let us know about any restrictions or financial terms we should take into consideration? Thanks, Astica. It’s a great question. We license AstraZeneca the right to use COM902 as part of their bispecific PD-1 and TIGIT and some other bispecifics. We fully own COM902. We do not 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, we remind all of us that in the days that the FC-active TIGIT initial deals were hundreds of millions of dollars of upfront deals. Being the probably only monoclonal FC-reduced TIGIT antibody out there, we believe that readouts in 2026 could bring meaningful interest back into TIGIT, especially in COM902. We have, again, we fully own it, so we can be fully opportunistic whatever direction we would like to take with COM902.
The next question is from Swampicola Rallicant of HC Wainwright. Please go ahead. Good morning, Yvonne and David. Thanks for taking my questions. A couple of quick questions. One is, when we look at the tolerability profile of COM701, how does that influence its potential use in combination therapies, especially in some of the less immune-inflamed tumors? The other question is, when we saw the data from the pooled analysis presented at ESMO, there were some grade 3 or higher treatment-related adverse events of about 16.7% or so. How do you plan to improve that safety in combination therapies? Michelle? Sure. Firstly, the tolerability of COM701 as a monotherapy is extremely well tolerated. In fact, we did not have any discontinuations due to adverse events in that pooled analysis when COM701 was used as a single agent.
In the triplet combination groups in the pooled analysis, the adverse events that were seen that were grade 3 were in keeping with the same frequency seen in the respective labels for both Nivolumab and Pembrolizumab. Given the tolerability of COM701 on its own, 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. Thank you. Thank you. Thanks for taking the questions. This concludes the Q&A session and Compugen’s investors conference call. Thank you for your participation. You may go ahead and disconnect.
This article was generated with the support of AI and reviewed by an editor. For more information see our T&C.