Compugen at Leerink’s Global Healthcare Conference: Strategic Insights

On Tuesday, 11 March 2025, Compugen (NASDAQ: CGEN) presented at Leerink’s Global Healthcare Conference 2025, outlining its strategic focus on immuno-oncology programs. The company, known for its computational discovery platform, highlighted both promising developments and challenges in its pipeline. The discussion centered on partnerships, clinical trials, and biomarker strategies, reflecting a cautiously optimistic outlook.

Key Takeaways

• Compugen’s collaboration with AstraZeneca on rilvegostomeg is advancing with multiple Phase 3 trials.
• The company is optimistic about its COM902 TIGIT antibody, with potential validation from rilvegostomeg’s success.
• There is a strong focus on biomarker strategies for better patient selection in trials.
• Compugen’s computational platform distinguishes it from other AI-driven approaches in drug discovery.

Financial Results

• AstraZeneca’s milestones and potential royalties from the rilvegostomeg program are considered significant for Compugen.
• No other specific financial results were disclosed during the conference.

Operational Updates

• AstraZeneca has initiated several Phase 3 trials for rilvegostomeg, targeting non-small cell lung cancer and gastric cancer.
• Compugen is conducting a Phase 1 trial for COM five zero three, an anti-IL-18 binding protein, in collaboration with Gilead.
• Plans are underway for a COM701 trial in platinum-sensitive ovarian cancer patients, focusing on those who have received maintenance therapy with Bev and SpA.

Future Outlook

• Compugen anticipates that the success of rilvegostomeg will enhance the validation and collaboration opportunities for the COM902 TIGIT antibody.
• The company is awaiting data from AstraZeneca regarding Winvego with ADC.
• Continued development of biomarker strategies is a priority to enrich patient selection in clinical trials.

Q&A Highlights

• TIGIT Program: Eran discussed the challenges with discontinuation rates and safety in other companies’ trials, noting lower activity levels than seen in preclinical models.
• Biomarker Strategy: Efforts are ongoing to develop biomarkers for responders, although prospective patient selection remains challenging.
• COM701 Trial Design: An adaptive trial with 60 patients, randomized two to one with PFS, is planned. A larger study will be needed for definitive conclusions.
• Maintenance Strategy: Various approaches are being considered, aligning with the current strategic path.

Readers are encouraged to refer to the full transcript for more detailed insights.

Full transcript - Leerink’s Global Healthcare Conference 2025:

Dana Greibosch, Senior Managing Director, Lyric Partners: Good morning, everybody. My name is Dana Greibosch. I’m a Senior Managing Director here at Lyric Partners, and I cover immuno oncology, and I have the pleasure of covering Compugen for several years. So thank you this morning to Eran, who’s the CSO of Compugen. We’re gonna do a fireside chat, and I’m gonna turn it over to Eran to give a quick intro of the company, and then we’ll get into the questions.

Eran, CSO, Compugen: Thank you, Dana. Thank you for having us. So Compugen is a clinical stage company focusing on immuno oncology and also a pioneer in computational target discovery. So we use a computational platform called Unigen to identify novel drug targets in the field of immuno oncology. Actually, we discovered TIGIT around the same time Genetec did.

And we discovered a few lanes to PVRIG, another first in class asset. And we have two wholly owned assets, COM701 blocking PVRIG, and COM902, which blocks TIGIT, the potential best in class antibody. And we also licensed to AstraZeneca the rights to use our COM-nine zero two as part of the TIGIT PD-one bispecific, and we’re going to discuss this trial soon. Also more recently, we identified another first in class IL-ten binding protein, and we developed a blocker antibody, COM-five zero three, which is licensed to Gilead. And we also have some more nondisclosed assets, all of them stemming from our computational discovery platform.

Awesome.

Dana Greibosch, Senior Managing Director, Lyric Partners: So I want to start with the program, the bispecific that you’ve licensed to AstraZeneca, because they have gotten incredibly aggressive with that program in the last year. And so the both the milestones and the potential royalties is pretty meaningful to Compugen. So, rilvelgostomeg? Do I say that right?

Eran, CSO, Compugen: Rilvelgo, then you

Dana Greibosch, Senior Managing Director, Lyric Partners: We’ll call it, you say, Rilvelgo? Rilvelgo, yes. Rilvelgo. It’s a TIGIT PD1 bispecific. It’s derived from your TIGIT antibody.

And they have many Phase three combos and they’ve started a lot of them in the last year. And I wonder, as you look across their portfolio of programs, is there any approach or trial that you have relatively more confidence given the data they’ve published today or by other, tungent molecules you think are relevant to theirs?

Eran, CSO, Compugen: Yes. So I think the most established data from them and from others is in the non small cell lung cancer, PD-one above fifty. So they actually showed really nice results encouraging more than sixty percent oral in these settings. So TROP and LUNG10 probably is interesting one in which they combine RILVEGO or RILVEGO plus that with the XT, their ADC, TROP2 ADC versus Pembroke in these settings. So I think this is definitely one to follow.

And also showed some nice data with gastric, also some other digit assets. So I think the gastric trial, for example, Artomide Gastric one, in which to combine Brilvego with Enerto, which is very powerful drug by itself, also interesting one. But to think also the others, I mean, Vela Retract, I mean, definitely, as you said, aggressive strategy kind of replacing the IO backbone with this PD-one digit bispecific is really fascinating for us.

Dana Greibosch, Senior Managing Director, Lyric Partners: Actually, maybe let’s talk about a couple of those. You mentioned the Tropium Lung ten and we talked about it after your last earnings, which is an interesting design from a milestone perspective, because I think it’s clinically derisked, even if TIGIT’s not necessarily adding anything because they have the bispecific plus their TRO2ADC, Datto DXD versus pembro. So you’re really stacking the deck. You have three mechanisms versus one. So clinically, it seems, very likely to be successful.

But I wonder if there is some regulatory or commercial risk to that. Regulators ask about contribution to components of both sides of the bispecific, that they don’t typically it sort of feels like this is going to push that question. If any trial pushes it, this might be one.

Eran, CSO, Compugen: Yes. Actually looking across the seven Phase three trials, most of them not necessarily compare RILVEGA to pembro. For example, in this ARTEMIDE, the GASP one, they are combining Rilvego with Enerto and chemo and they compare it to pembro plus Herceptin plus chemo. So in this trial, they’re not really comparing directly Rilvego to pembro and also in most of the other trials. So first of all, I don’t know.

I am not part of the discussion with AZ and FDA. I just got to assume that they are building these trials toward approval. And they do expect to see that if the risk benefit profile and what is great about Wilvega, not only it’s effective, but it’s also as a very having a non active FC has a very good safety profile from what we’ve seen until now. So it’s a very good combination partner. So overall, probably what they will have to show is that if the risk benefit of adding Wilwego to talk to ADC versus Prenbo is going to win, both in terms of benefit, but also in terms of the risk, they’ll probably get approval.

But again, this is not we’re not part of the discussion with the FDA and AstraZeneca. Just our view on that.

Dana Greibosch, Senior Managing Director, Lyric Partners: There’s another interesting component of this, which I’d love your opinion on because you do so much work biomarker and AI wise. But they’re using this biomarker, the TROPE-two QCS, which they developed with AI also to enrich patients in that trial. I think, you know, some of the concern we’ve heard from investors and KOLs is that they develop that biomarker in a post hoc manner and that then they’re using it prospectively here, but how validated is it really could they be chasing a signal? And I wonder if you have any thoughts on that?

Eran, CSO, Compugen: Yes. So normally, every biomarker start by post hoc analysis and defining criteria. Obviously, at certain points, you need to prospectively select patients based on the biomarker. So there is always a risk. But I think from my experience, since you shouldn’t have any much of bias doing this retrospective analysis, if you’re doing it right, and I’m sure they are doing it right.

So I think the risk is not huge. But yes, you definitely need to see how it works in prospective selection of patients based on the biomarker and the sophisticated AI based approach, we’ll have to see how it works. I’m positive on that in general.

Dana Greibosch, Senior Managing Director, Lyric Partners: Both the trials you mentioned, the gastric one and the lung, have an ADC component as they’re taking it forward. And have we seen any data with ReVelGo and ADCs? And then sort of more theoretically or from your preclinical work, do you expect mechanistic synergies with TIGIT and ADCs, anything different than PD-one alone with ADCs?

Eran, CSO, Compugen: Yes. First of all, we will see this here according to AstraZeneca data, some initial data from combining Winvego with ADC, so definitely eager to see that. Well, I’m not sure if there’s something specific. We know that the ADCs, which are eventually smart chemotherapies, are inducing immunogenic cell death and reduced tumor burden. So there’s synergistic with checkpoints in general.

I’m not sure if there’s something when some chemo might increase the expression of PVR, but I’m not sure specifically these ADCs. So overall, I would assume it should be synergistic at least like with PD-one and other checkpoints. I’m not sure of something specific for Tejets there.

Dana Greibosch, Senior Managing Director, Lyric Partners: That’s interesting. Maybe we should tell everybody what PVR is.

Eran, CSO, Compugen: Yes. PVR is the ligand of Tejets, yes.

Dana Greibosch, Senior Managing Director, Lyric Partners: Yes. Thanks. And so interesting. Let’s I guess, moving to your own COM nine zero two program, sort of what read through do you see from Ravel Go to your own program, given it’s half, it’s half of the bispecific? And as you think forward, if the bispecific works, it has all these regulatory advantages and it has AstraZeneca, investing behind it.

Where could you find success with COM902 that would have already been taken by Ryvergo?

Eran, CSO, Compugen: So I think there is definitely a direct impact on nine zero two, because nine zero two, like Ryvergo, is an FC reduced binding, so the same class of digit antibodies and eventually the same digit antibody. So successors, Ryvergo definitely going to reflect on nine zero two and actually make it a validated clinical asset. There are quite a few opportunities. Obviously, other companies who might want a good best in class potential TIGIT antibody could have an interest there. For all combination, when we add COM701, we discussed this soon, that two PD-one and TIGIT, this actually opens the door to take what we believe and started to show taking TIGIT and PD-one into less inflamed indications.

So this is something that we could do with COM902. So I think it will be great for COM902, both from our own internal validation and moving with the target and also as a potential asset for collaboration with others.

Dana Greibosch, Senior Managing Director, Lyric Partners: Let’s talk about your PVRIG antibody COM701 and maybe we come back to TIGIT, but I want to make sure we talk about it. Can you summarize the data that supports that PVRIG will prove to be an important IO target in ovarian cancer, which is where you are developing it, particularly as other IO therapies have had a little bit of activity in ovarian, like a glimmer multiple of them, PD-one, IL-two, CTLA-four, but that really hasn’t justified ever later phase development.

Eran, CSO, Compugen: Yes, ovarian is definitely a tough one for immuno oncology and there are many attempts and not many success. So there are few good reasons why we think we should be different with COM701. First is biology. The PVRG pathway is highly expressed in ovarian. It was target indication for us from the beginning.

And we think that this is a good indication to test PVRG in general blockade in general. And then looking at the biology of specifically PVRG compared to other checkpoints, it has a very different biology. And its biology, which relates to its expression of stem like memory T cells and dendritic cells, has shown to increase inflammation in less inflamed tumor types across few indications. So this unique biology should be able to drive T cells in a less inflamed indication like ovarian cancer. And what we saw across all our trials of signals activity in places which checkpoints are typically not working.

So there’s a biological reason to think why PVRG blockade could work where the other checkpoints work. And then the clinical data, which is probably the most important, the proof is in the pudding. So we didn’t test many patients in monotherapy, only six, but one of them responded long term duration of response to PVRG2COM701 and three more were stabilized by monotherapy treatment and all the translation signals showing that we are able to modulate very effectively tumor environment in ovarian cancer patients, last line platinum resistant patients with monotherapy. And then looking at the triplets, I mean, historically, as you said, PD-one even PD-one plus digits showed eight percent response rate in platinum resistant ovarian cancer. We tested 40 patients and we had roughly twenty percent response rate.

So and the reason we did 40 patients, we wanted to make sure that yes, we are above that signal of the PD-one plus digit. So we have the biology and we have the clinical signals that COM701 blockade and mono or combination is active in platinum resistant ovarian cancer patient. And And these are heavily protruded patients. Some of them attempt few clinical trials before even entering our trial. So now the rationale is, let’s go earlier into the platinum sensitive settings.

We identified this group of patients, which are second or third line. They already received maintenance with Bev, already received maintenance with SpA, but you cannot tolerate it. And this patient received the platinum chemotherapy and like the six cycles, and then they’ll just sit and wait to become platinum resistant. They don’t have any maintenance option there. So we have COM701 with its clinical signal, excellent safety profile and the patient who did respond in our trial showed really extremely long duration of response.

So this is exactly the type of drug you want in this maintenance settings. And this is why we’re doing our trial in these settings. And also, by the way, the competitive landscape in the platinum sensitive setting is completely different from the platinum resistant to which the ADCs are now very moving aggressively into that indication.

Dana Greibosch, Senior Managing Director, Lyric Partners: Maybe if you follow-up, do you know why ovarian present with high PV or Ig, is imply something about the immune cell composition within the tumor?

Eran, CSO, Compugen: Yes, it’s a good point. We are not sure. What we’ve seen is that in hormone driven indications like breast, endometrial and ovarian, for example, we do see up regulation of the ligand, PVRL2. I remind you that, for example, we had complete response in HR positive breast cancer patients, we had responses in endometrial. So we do see also clinical signals in these indications.

And PVRG itself with its expression of stem like memory T cells, there are new publications show that platinum actually induce TLS and stem like memory T cells. This also suggests why we think it will synthesize the tumor to response to COM701. So this might explain also why PVRG itself is relatively high in ovarian cancer. So we’re not sure, but definitely we see dominance of the pathway in ovarian cancer in general.

Dana Greibosch, Senior Managing Director, Lyric Partners: Actually, I’m sure you understand. So is it both the ligand, PVRO2 and PVRO2?

Eran, CSO, Compugen: Most of them are relatively high, yes.

Dana Greibosch, Senior Managing Director, Lyric Partners: That are relatively high. Yes. Interesting. You early on had pretty interesting biomarker data that showed that patients that expressed the ligand you had an enrichment of clinical benefit. That was in the first twenty patients, I think, or an early cohort.

Are you still developing that biomarker as you move forward? And what can we learn from this next study in the platinum sensitive population about that biomarker and enrichment strategy?

Eran, CSO, Compugen: Yes. So obviously, again, going back to our results, we had these patients who responded really nice to the drug and some who have actually less benefit. So we looked retrospectively, we used all our tools, computation analysis, because obviously the holy grail is to identify this population of patients. And we have initial observation of PVRL2, the lagoon of PVRLG being able to be highly expressed on patient who responded. We had similar observation in a small breast cancer cohort.

So it was interesting, it’s really important. But at this point in time, we don’t have sufficient data to really start prospectively select the patients. So we’re going to continue to follow. It’s a bit more challenging in the pattern sensitive because the availability of really pre treated biopsies is not as abundant as you can get in the late light settings. But we’re definitely going to continue follow-up on that because this is critically important and the signals were there and we just need to substantiate it much more before we start prospectively selecting.

Dana Greibosch, Senior Managing Director, Lyric Partners: So you’re not going to require biopsies to enroll because we don’t want to slow down?

Eran, CSO, Compugen: Yeah, we cannot. In these settings, we probably going to have some archival and whatever we can get, but it’s not going to be a mandatory pre treatment biopsy probably.

Dana Greibosch, Senior Managing Director, Lyric Partners: Is there anything you can look at sort of in ctDNA or in liquid biopsy, the CTCs?

Eran, CSO, Compugen: We didn’t disclose all of that. But obviously, as we always do, we put a lot of efforts in the translation. CtDNAs are not clinically validated in ovarian, which is definitely could be an explore to readout we might consider to explore to support the clinical readouts.

Dana Greibosch, Senior Managing Director, Lyric Partners: Got it. What gives you confidence that COM701 will have single agent activity in this platinum sensitive? You previously were building and building to doublets to triplets and now going back to a monotherapy.

Eran, CSO, Compugen: So first, the biology and the clinical signals we have seen in monotherapy in platinum resistant ovarian cancer. And then moving to the early settings, we know that this that looking at the swivel plots in our study, you see some of the patients responding really long term and deep responses. And some of them in the platinum resistant settings, again, after so many trials, so many failures, they progress so fast. I mean, they probably never had the chance to respond to a treatment which is chemotherapy free, like the one we used. Now going to the platinum sensitive, having a debulking first, we’re going to take only the patients who responded to the treatment.

So they have low tumor burden. They have been synthesized by the platinum probably to respond better to COM701 due to this TLS and TSCM. And in this early line also the immune system in general is probably more functional. So I think that while we’re not able to enrich biomarker BVAR2, we think that we are going to enrich for responders by looking at this line of treatment after responding already and have low tumor burden to the platinum. So this is the rationale and think we have a good I I mean, we have a good reason to believe it should work, but definitely we didn’t test it yet in the platinum sensitive and we have to wait and see.

Dana Greibosch, Senior Managing Director, Lyric Partners: Maintenance feels like a very natural place for any checkpoint inhibitor or immune therapy, because we know that tumor burden in patients of high tumor burden is, I think, maybe consistently the most correlative clinical signal to lack of response. But we haven’t seen that many companies use this path. Now there’s adjuvant post surgery, so early stage that’s certainly a path. And, Mercaga and Pfizer used it in bladder cancer. But it hasn’t been used very many other places.

And I wonder if you could speculate on why? And does that introduce any risk that it’s a less trodden path?

Eran, CSO, Compugen: I think in general, I mean, for checkpoints and also for other clinical development, many times you look for the signal in the last line settings and then you move earlier. I mean, also in the last three, it was of maintenance, but they saw some signals in the relapse setting and then they move to the first line melanoma trial. So I think it makes sense. I think that specifically that population that we identified in ovarian, We had tons of discussion with KOL to really identify this exact population, exact unmet need, and we’re really glad we’re able to identify it. So I think it’s and there are some trials, for example, the GLORIOSA trial, did try ADC plus Veb versus Veb, not exact same patient population, but people are looking different attempts from maintenance.

Specifically for checkpoints, I mean, there are some approvals and again, in a way, it resembled the adjuvant settings and but I think this is definitely a place that makes sense. And specifically, we believe that PVRG is such checkpoint that should work in ovarian where other checkpoints failed in maintenance settings in ovarian till now.

Dana Greibosch, Senior Managing Director, Lyric Partners: One concern we have about the study is you’re using PFS as a primary endpoint. It’s randomized, which is nice, but you only have 60 patients randomized two to one with PFS. And PFS overall, but in this setting, if you look historically, is quite variable. And so I guess the worry is that you don’t end up with a balanced population, in the two arms and it will be difficult to interpret. Why am I wrong?

Eran, CSO, Compugen: Yes. Well, you’re not wrong. Obviously, if we do a 300 patient study, then we have more robust results and we could make you do clearer conclusions. But to think, even though we’re quite confident in the signals which you’ve seen in monotherapy and in the biology, we’re now entering for the first time to platinum incentive settings. This patient population is really defined.

We’re really focusing on unique, so we think that the chances for bias are relatively small. The historical control for this population is very stable across few Phase three trials, so we know what to expect. And then we also have the internal randomized control. So based on our discussions with KOLs, with Biostats running the simulation, we think that this size of study should be sufficient to enable us to reach into a conclusion. The conclusion with a relatively you also have the risk of false positive, false negative, but statistically, it’s going to be sufficient for us to make a decision with high relatively high certainty.

And then we can do few things, because this is an adaptive trial design. Either the trial is futile, okay, so it’s good to know that we don’t see signal there. But if we do see signal, we expect for three months progression of PFS. If we do see signal, then we can do a few things. The way the trial is designed, we can continue to enroll more patients and consider now going with regulatory authorities to go into the fast track approval.

We can stop the trial and say, okay, now we have estimation of the magnitude of effect. We can start now design our properly Phase three study or we can now add other combinations. This is exactly the DAPT trial. We can add BAB, we can add triplets and then see what happens. So I think this trial design is exactly sufficient for us to making early conclusion to see where it goes and then we are quite flexible on the next steps.

Dana Greibosch, Senior Managing Director, Lyric Partners: There is one other IO drug in Phase three right now in ovarian. It’s Mural Oncology. It’s nimbleukin alpha, which is not alpha IL2. They’re combining with pembro and platinum resistant ovarian cancer. If that happens to be successful and I think it reads out this year, would that change anything about how you’re thinking about COM701?

Eran, CSO, Compugen: So first, I think they’re going to the platinum resistant centers. We’re going early to platinum sensitive. There’s not going to be direct competition. But looking at the decision making they made, it’s interesting to see because I think overall, they treated that data for 14 patients and the confirmed response rate as far as I’ve seen is roughly as ours, twenty percent. And then make they made a decision, which is obviously, I mean, they took a risk, but obviously a decision that could we could have taken as well to start a big Phase three trial in this setting of vitamin resistance.

And we took a different route to say, okay, we think that it’s a bit more challenging for a chemo it’s chemotherapy free, especially given the ADCs competition to remain in that settings. And we thought we have higher chances to move into the earlier settings in the maintenance settings. So first, it’s not that there are competition for us, definitely interesting to see, but just a different strategy.

Dana Greibosch, Senior Managing Director, Lyric Partners: Got it. You wouldn’t then combine a IL-two for instance or you could consider that later on anyways.

Eran, CSO, Compugen: Maybe with COM5 with

Dana Greibosch, Senior Managing Director, Lyric Partners: And your adaptive trial. Yes. Let’s move on to TIGIT. A couple of questions there because I do want to get to, your IL-eight team binding protein as well. What happened with Merck?

You’ve been in TIGIT and thinking about TIGIT for a very long time, and we haven’t seen the data yet. I think a lot of investors say, look, Dana, isn’t the simplest explanation likely true? Digit is just not that good of a target.

Eran, CSO, Compugen: So first of all, not all digit antibodies are the same. And we started discussing the efficacy issue. So Genentech eight mirrors that were the first movers in the field also generated the first important results have an active FC. An active FC is associated from what we see with nobody did a direct comparison, but across trials, different safety profile, higher discontinuation rate compared to the non active FC like we and AstraZeneca and ARKOS had. So not all digital is same.

But also what you also know that TIGIT is probably is active. I mean, few randomized Phase two studies have shown that digits is an active molecule. The question is how activities and given there also some safety issues, especially BFC non active, the risk benefit of using TIGIT becoming more challenging, especially when you have an active IFC. This is my take on that. So and especially for Mac with the DIT core formulation, we cannot even discontinue TIGIT alone because it’s core formulated.

So I think definitely the activity of Trigid is not what we have seen in the mice. It’s synergistic with PD-one and melting tumors, but it is an active molecule and with the right FC, it’s a very good combination partner for PD-one and AZ strategy. And what we are trying to do, I think, is different from what Merck and Genentech try to do.

Dana Greibosch, Senior Managing Director, Lyric Partners: Is there anything in particular you’re looking to validate that hypothesis when Merck does share the data?

Eran, CSO, Compugen: We saw quite extensively the discontinuation rate also for other companies with active Fc. I assume we’re going to see the same. We’re going to see the safety. We’re going to see discontinuation. Also in terms of efficacy, one might imagine that if you have an active Fc that have the potential to deplete the same cells you want to reinvigorate by tigid blockade, maybe even the efficacy is harmed by the active FC.

But I assume we’re going to see the more of the same in terms of the active FC for

Dana Greibosch, Senior Managing Director, Lyric Partners: Yeah, like really like to see all their T cells and how the compartments change. They’re probably not going to show us that. Probably didn’t even measure that.

Eran, CSO, Compugen: I mean, not in the phase three trials.

Dana Greibosch, Senior Managing Director, Lyric Partners: Let’s talk about COM five zero three. That’s your anti IL-eighteen binding protein that you’ve licensed to Gilead, but you’re running the Phase one trial. And I wonder just could you tell us why you’re excited about this approach, and any expectations we should have for the Phase one in terms of the kind of signal you expect?

Eran, CSO, Compugen: Yes. So, RTMP is a great example of demonstration of computational capabilities, because we looked for resistant mechanisms of TAMs in tumor co environment computationally. We’re not looking for a cytokine therapy at all. And we identified in unbiased manner that we have a resistant mechanism in tumor environment called ILTMP. It was identified before, but we identified that by using a blocking antibody, we could have a very different cytokine approach compared to all the other cytokines, because cytokines are amazing in inducing in vitro stimulation of immunity.

But when you give into the blood, normally in high levels, they have a real challenge and practically so many developments failed, like the Nektar and others trying to really reach sufficient amount of cytokine in the tumor environment before you induce first toxicity in the periphery. So these are all the failures of cytokines and probably challenges that also the next generation ILT molecules, which doesn’t bind ILTENBP might face as well, because it was also given systemically to the blood. What we identified that in a tumor environment, you have IL-ten naturally there because it’s induced by phlammasome signaling, very low in the periphery, but it’s not active. So you have very potent cytokine floating in the tumor microenvironment bound by this IL-ten binding protein molecule, which inhibits it. So we’re using we use a blocker antibody and drug moiety.

We inhibit the inhibitor. So we displace IL-ten BP away from IL-ten. And by that, we induce localized activity of the cytokine mostly almost only preclinical in tumor convironment. So we started now the Phase III trial. This asset was, as I said, has mentioned, licensed to Gilead, but we are leading the Phase I trial.

And we just started those escalation. And from our clinical data, we expect to see a very differentiated activity, probably TME localized effect, hopefully to see some monotherapy signal as we’ve seen pre clinically. Yes, we’re excited to do this study.

Dana Greibosch, Senior Managing Director, Lyric Partners: Are you getting the paired biopsies to observe that local TME effect and understand your dose window? So we didn’t disclose all

Eran, CSO, Compugen: of that. We you can see in clinicaltrials.gov that we have a backfill courts. So typically people are doing in backfill some dose optimization. And looking for what they did for other studies, one might speculate that we’re going to put a lot of efforts as we did for COM701 in on treatment biopsies, sequencing, using Orec potential capabilities to really understand the drug MOA, biomarkers and potential PD markers. So but this is not disclosed specifically for this program yet.

And this is in cooperation with Gilead, so we’ll see about disclosures.

Dana Greibosch, Senior Managing Director, Lyric Partners: Yes. Are there any particular indications that have high IL-eighteen binding protein that you’re are you trying to enrich those or would you enrich in

Eran, CSO, Compugen: the future? So actually, we have seen and also published that IL-ten BP and IL-ten, I mean, this complex of IL-ten mostly bound to IL-ten BP is quite abundant in many indications. So we’re not sure if the levels of IL-ten or IL-ten BP are going to be limiting. We did see that preclinical unit some amount of T or NK cells to respond to the initial burst of IL-ten released by the drug. So probably a good start will be not completely desert tumors, but the opportunities are quite broad across many indications.

Dana Greibosch, Senior Managing Director, Lyric Partners: Maybe last question. Your discovery platform, you talked already about how the computation helped you discover IL-eighteen. Can you talk more in a forward looking way? And how is your platform and your AI work different from what we’re seeing others do right now with an AI explosion? You’ve been doing it forever.

Eran, CSO, Compugen: Yes. Exactly. So we’re doing it for quite a while. And I think it’s sometimes difficult to explain the exact tools. But what is easier to see is that our platform is validated.

I mean, many people claim that can discover new drug targets by using AI, not many have shown. And we discovered TIGI, we discovered PVRG, we discovered ALDA2, we discovered ILTIM BPA as a drug target for for a blocker antibody. So multiple times we have shown that using computational capabilities, we can identify and bring novel drug targets are very few, if any companies who have such track record computationally. So I think eventually the proof is in the pudding and this is what differentiate us that this is a validated platform to identify novel drug targets.

Dana Greibosch, Senior Managing Director, Lyric Partners: And with that, I guess one last question, back on Tigit. We talked about how, Astra as well as Arcus Gilead have FC incompetent digits. But I do know that COM nine zero two is differentiated from Arcus’ TIGIT. And I wonder if you could just tell us a moment of how it’s differentiated in case both those are successful and how that differentiation could prove out for you?

Eran, CSO, Compugen: So I’m not sure we compared directly to Arcus, but we did test in the past the affinity of the CAR REN2 versus most of the other leading benchmarks. It has it’s just a very good antibody, probably that’s why AstraZeneca chose it. So it has a very good binding affinities, blocking capabilities. And the Fc is not exactly the same, but I don’t I’m not think it’s very different. It’s IG4 versus with IG1.

So maybe have some very low Fc binding. Clinically, I’m not sure if all of that is going to translate to meaningful differences, but we’ll have to see.

Dana Greibosch, Senior Managing Director, Lyric Partners: Got it. Okay. Thank you very much. Thank you, Dana. Thank you, everyone.

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