Compugen Ltd (CGEN) 2025 Q3 法說會逐字稿

Ladies and gentlemen, thank you for joining us today. Welcome to the Compugen Third quarter 2025 results conference call. (Operator Instruction). I would now like to introduce Yvonne Naughton, VP Head of Investor Relations and Corporate Communications.

Thank you operator, and thanks everyone for joining us today. Here with me from competent team are Eran Ophir, our New President and CEO, and David Silberman, our Chief Financial Officer. Michelle Mahler, our Chief Medical Officer, would 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 on Form 20.

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 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.

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 digit biology is now gaining clinical momentum.

I think that now is a great time to highlight what makes us different in the digit drug development space and why you should be paying close attention to our differentiated FC reduced anti-Tigid programs and their advantages over FC active anti-digid 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-digit 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 digits can deplete digit positive effector T cells and Tregs, and this is not desired because one, on efficacy. Digit is present on effector T cells.

So similar to the action of antiPD1s, you want to reinvigorate these exhausted cells and avoid their depletion.

two, on safety, digit is present on Tregs, depleting peripheral Tregs could result in immune-mediated side effects.

FC reduced antitheids like our own common NO2, in contrast, preserve and reinvigorate effect of 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 early as phase 2 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 3 trials. For example, during recent EMO meeting, the presenter highlighted that in Skyscraper 07 trial, adding FC-active digit to atezolizumab resulted in these patients only receiving median number of doses of 12 versus 17 in the Atezo-only arm.

As a result, the patients receiving digit PDL1 combination received 30% less the PD1 antibody versus control.

So safety really impacted the ability to administerrate treatment and therefore probably impacted the outcome.

We've always advocated for the EFSI reduced formats, and we believe that the data is starting to support our convention.

Not all anti-digit 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 digit programs.

(Inaudible) It is one of the only two clinical stage FC reduced anti-treated monoclonal antibodies currently in clinical development, and importantly, it's fully owned by Compugen.

Positive phase three 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 com 902.

Notably, recent overall survival data from their phase 2 frontline gastric cancer study, which is the same setting as the Arcus Gilead ongoing phase 3 trial, was presented at EMO recently and showed the media 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 reducedanti-PD-1/TIGIT, with the digit component derived from our FC reduced high affinity comm 902.

Interestingly, cooperative by specific binding might provide even further efficacy.

Into PD1 and digit blockade while in addition potentially supporting an easier regulatory path.

The potential commercial opportunity for will be substantial, with AstraZeneca estimating non-risk adjusted peak year revenue target of more than 5 billion.

We understand that AstraZeneca's ambition is for to replace PD1 PDL1 therapies.

And to serve as the backbone for future combination treatments.

Their broad development program spanning 11 phase 3 trials across lung, gastrointestinal, and endometrial cancers represent a potential significant value drive 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 monoclonal anti-PVRG antibody in the clinic, which again, we believe is the right FC format.

The biology here is truly differentiated from PD1 and TG checkpoints, providing advantages that we believe could translate into clinical benefit for patients with platinum sensitive ovarian cancer.

Positive data in our ongoing Maoviron platform trial could support a broader clinical development program aimed at addressing a significant unmet medical need.

And finally, to our cool and smart potential first in class antibody program addressing cytokine biology. GS- 0321, previously 03, is a potential first in class anti-tin binding protein antibody licensed to Gilead.

GS-0321 represents a novel antibody approach to harness IL-T path by bi biology for the treatment of cancer, potentially.

Overcoming the limitations presented by the administration of therapeutic cytokines.

It represents another potential value driver for Compugen, as you're eligible to receive 758 million in milestone payments and single-digit to low double-digit tilled royalties. This program is the most recent example of how our AIML 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're committed to delivering real breakthroughs, not just incremental therapies, and real innovation is never easy. It takes time, persistence, and willingness to tackle the toughest scientific challenges.

But I believe deeply in what we are doing here, and we have the best talent and great tools to do this, and 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 ESO in Berlin in October where we presented a pool analysis of our three previously reported phase 1 trials reflecting the clinical benefit of 701 as monotherapy and in combination in patients with heavily pretreated platinum resistant Ovarian Cancer.

The pool analysis demonstrated that com 71 was well tolerated, showed consistent, durable responses in patients with heavily pre-treated plain resistant ovarian cancer, particularly in those without liver metastasis, representing patients with lower disease burden in a potentially less immunosuppressive tumor marker environment.

The results of the analysis support the rationale for the ongoing randomized myoarian platform trial evaluating com 701 is maintenance therapy in early lines of treatment.

The Mayo Van Platform trial is progressing. Sites have been activated across the US, Israel, and France, including major academical centers and multiple sites from the French Oncology Cooperative Group Arkady Gico, renowned for several recent platinum sensitive ovarian cancer trials.

We now estimate the interim analysis in Q1 2027. We believe my 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 Rilve data at ESO as part of two mini oral sessions. Arma01 follow-up showed that Rilve 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 supports differentiation of the FC reduced formats.

The Tropion Pant tumor 3, evaluating combination of rilve with DA showed promising efficacy and manageable safety, underscoring the potential of next generation Ibispecific plus ADC.

Moving next to GS-0321, our novel antibody approach with Gilead that leverages cytokine biology, the phase round trial is progressing as planned and represented la trial design at CII 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 up 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 com 71 platinum sensitive ovarian cancer trial, Maya Ovarian, and to support the progression of ZS0321 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 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 proceeds 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 ID 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 GN 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 Instruction) Stephen Willey, Stifel.

Yeah, good morning. Thanks for taking the question. Just curious, the extension of the Maya intern analysis from I guess the second half of 26 into the first quarter of 27 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, Steph. So, overall, as we know, there are a few factors that determine the initial readouts of clinical trials. It's opening the sites, is the actual enrollment rates, and finally, the actual accumulation of events along the trial.

And we start the trial by giving an estimation, and the more the trial develops, you understand the kinetics and you optimize your prediction. This is exactly what we're doing here. We can say today that we opened most of the sites, including major academical US centers and the French Acaio Guinco Group. It took a bit more time to open. It's mostly the 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 an open and adding the French sites also was done because they showed interest and also to support the aggressive enrollment rate that we anticipate.

And now this is the time for the start enrollment and see the actual ramp up and Michel, if you want to add something to add some color.

No, I mean you've 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 bit longer to open. In addition to that, we had also been consulting with Gico in France when they asked to participate as well, so. You know 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.

And finally, we also disclose today that we have cash runway into Q3 27, so we also have the cash to support the taking into account this shifting to Q1. So to in a good position to continue with the Maya trial and to bring value for patients because we think and we believe in this study.

All right, thanks for taking the question.

(Operator Instruction), Daina Graybosch, Leerink Partners.

Hi, thank you for the question. I wonder if we could talk about the upcoming Arcus, Gilead Rita with their TIGIT and 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 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 bis specific, Rovigo.

Thanks, Daina. It's a very good question. So, this will be the first phase 3 readout for an efficiency reduced digital antibody. The data in Israel looked promising, but it was a single arm study, not many patients, but doubling, or almost doubling the overall survival versus stroke on control was reassuring.

And now is the time to see how it evolves in the phase 3, and this is, of course, could be very meaningful for us.

But it is only one 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 three readout. But even if this trial fails, Arcus Gilad himself had an additional phase two, phase three trials, additional two ones, and AstraZeneca has two additional advantages over the, just a single monoclonalef reduced. One is they show that the revised specific has a potential.

More activity and actually showed it in a very nice Xvivo patient derived material system and they have a cooperative binding that allow cooperative blockade of PD1 and digit on the same cell, and the result was in that relatively translational system that it's more active than just PD1 and TIGIT blockade.

And then also in some of the trials, the other potential regulatory advantage is the way we see it looking just for the size of all the accumulating phase three trials. For example, in one of the trials in the, I believe it's the (Instruction) 01, they're comparing Rilve plus chemo to just chemo, and because it's a bi-specific, nobody can ask for a contribution of components as far as we understand it. And therefore you don't need to show that digit is active. Yes, we believe digit is active and they have reduced, but even if the activity is not sufficient, in this case, having involves enhanced efficacy. Due to the bi-specific format and just using it as an IO safe backbone to combine with chemo to compare versus chemo, this is definitely an advantage of the BS Pacific. They have some other trials doing the same, and they also have some trials doing directly head to head versus Pembroke, 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 bi-Specific indeed.

(Operator Instruction) Leland Gershell, Oppenheimer & Co Inc.

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.

So I will start and then over to Michelle. So again, just to remind everyone, we talked about a study which has 40 patients treated with com 701 in maintenance settings compared to 20 patients in placebo. We're relying on a solid historical control and internal control, compared 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. 71 has a monotherapy signal in this patient population after seeing a signal in the last line plattoum resistant settings, 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 accelerate approval, and Michel, 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 com 701. 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.

Great, thanks very much.

(Operator Instruction), Asthika Goonewardene, Truist Securities.

Hey guys, good morning. Thanks for taking my question. So, with comm 902, this would have to be an unpartnered actually reduced digital antibody, in the wake of, new data coming up from, the people we're watching on ourcus and making readrs here. So, I know you've 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, Asthika. It's a great question. So, we license AstraZeneca.

The rights to use com 902, a part of their by specifics, PD1 and digits, and some other bi-specifics, but we fully own com 902. 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. We remind all of us that in the days that the FC Active digit initial deals there were hundreds of millions of dollars of upfront deals.

And being the probably only monoclonal FC reduced digit antibody out there, we believe that readouts in 26 could bring meaningful interest back into digits, especially in com 902, and we have, again, we fully own it, so it's, we can be fully opportunistic whatever direction we would like to take with com 902.

(Operator Instruction), (inaudible).

Good morning, Eran and David. Thanks for taking my questions. Couple of quick questions. One is when we look at the, tolerability profile of com 701.

Well, how does that influence its potential use in combination therapies, especially in some of the less immune inflamed tumors?

And, the other question is, when we saw the data from the pooled analysis, presented at AS, there were some grade three or higher, treatment related adverse ones, about 16.7% or so. So how does, how do you plan to, improve that safety, in combination therapies?

Sure, so firstly, the tolerability of comm 701 as a monotherapy is extremely well tolerated. In fact, we didn't have any discontinuations due to adverse events in that pooled analysis when comm 701 was used as a single agent and in the triplet combination groups in the pooled analysis.

The adverse events that were seen that were grade three were in in keeping with the same frequency seen in the respective labels for both nivolumab and pembrolizumab, given the tolerability of com 701 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.

Okay.

Thank you. Thanks.

(Operator Instruction).