Ladies and gentlemen, thank you for joining us today. Welcome to Compugen’s First Quarter 2023 Results Conference Call. At this time, all participants are in a listen-only mode. An audio webcast of this call is available in the Investors 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, 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 for Compugen for the prepared remarks are Dr. Anat Cohen-Dayag, President and Chief Executive Officer; and Alberto Sessa, Chief Financial Officer. Dr. Henry Adewoye, Chief Medical Officer; and Dr. Eran Ophir, Senior Vice President Research and Drug Discovery 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 its programs, financial and accounting related matters, as well as statements regarding the company’s future cash position. 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 the SEC filings for more details on these risks, including the company’s most recent annual report on Form 20-F, filed with the SEC on February 28, 2022. The company undertakes no obligation to update projections and forward-looking statements in the future. And now, I’ll turn the call over to Anat.

Thank you, Yvonne. Good morning and good afternoon, everyone, and welcome to our first quarter 2023 update. At Compugen, we are advancing a differentiated clinical strategy evaluating a drug combination that was never tested before in a space, where there is a significant unmet need and potential opportunity to transform the lives of cancer patients with the right immunotherapy combination. Compugen has always believed that in certain patients and in certain tumor types blocking the three pathways of the DNAM axis PVRIG, TIGIT and PD-1 may be needed to enhance antitumor immunity. We have always said that blocking TIGIT in addition to PD-1 may not be enough, a concept that is now increasingly reflected in the consistent move of larger pharma players to add an additional drug to the TIGIT/PD-1 drug combinations in various indications. Given the potential of PVRIG inhibition to sensitize tumors to PD-1 and TIGIT blockade, we believe the biological and mechanistic rationale support the addition of an anti-PVRIG to the anti-PD-1/TIGIT mix, and we have the initial clinical and translational data to support our hypothesis. We are the leaders in the unique chemotherapy three [ph] triple combination approach of blocking the three genome access immune checkpoint, PVRIG, TIGIT, and PD-1, and we are focused on maintaining this leadership. We have initiated 2 follow on proof-of-concept studies in indications not typically responding to immunotherapy, microsatellite stable colorectal cancer and platinum resistant ovarian cancer. The former is enrolling patients and the latter is open for screening of eligible patients. In these difficult to treat indications refractory to standard of care, we have previously demonstrated encouraging clinical benefits, including in-patient refractory to anti-PD-1 and in in-patients whose tumors were immune desert. These data are supported by immune activation that aligns with COM701 mechanism of action. The goal of the…

Thank you, Anat. I’m happy to summarize our financial results. I will start with our cash balance. As of March 31, 2023, we had approximately $74.3 million in cash, compared with approximately $83.7 million as of December 31, 2022, affirming our focus on capital efficiency while continuing our bold execution on our DNAM-1 axis hypothesis. The company has no debt. We recognize the importance of cash efficiency and we are disciplined in how we deploy our cash resources, making sure we will focus on reaching key milestones with our available cash runway at least through the end of 2024. It is important to emphasize that this does not include any potential cash inflows, including potential milestones payment from our collaborator AstraZeneca. The timing of milestones payment will depend on the progress of studies run by AstraZeneca. For contractual reasons, we cannot provide the breakdown of the milestones payment. To remind you to date Compugen received development milestones payment of $2 million, $6 million and $7.5 million for achieving preclinical milestones and for dosing the first patient in Phase 1 and Phase 2 studies, respectively. Compugen is entitled to receive an aggregate of up to $200 million in development, regulatory and commercial milestone for the first product. Expenses for the first quarter of 2023 were in line with our plans. R&D expenses for the first quarter of 2023 were $7.4 million, compared to $7.2 million in the first quarter of 2022. Our G&A expenses for the first quarter of 2023 were $2.6 million, compared to $2.6 million in the first quarter of 2022. For the first quarter of 2023, net loss was $9.3 million, or $0.11 per basic and diluted share, compared to a net loss of $9.7 million, or $0.11 per basic and diluted share in the first quarter of 2022. With that, I will hand back to Anat to summarize.

Thank you, Alberto. To summarize, we are on track to present initial findings from 2 studies evaluating our leading triple combination blockade of PVRIG, TIGIT and PD-1 by the end of this year. These studies are building on prior data suggesting that blocking PVRIG may sensitize tumors to respond to PD-1 and TIGIT blockade and could turn cold tumors hot, potentially offering a chemotherapy free option for tumors most competitors are not targeting metastatic MSS CRC and platinum resistant ovarian cancer. This is a real potential opportunity to transform the lives of patients with the right immunotherapy combination. With that, I will turn the call over for questions. Operator?

Thank you. Ladies and gentlemen, at this time, we will begin the question-and-answer session. [Operator Instructions] The first question is from Mark Breidenbach of Oppenheimer. Please go ahead.

Hey, thanks for taking my questions and congrats on the quarter. Just a couple of quick ones from me. I was wondering if you could comment on any potential read through between observations you’ll be presenting at ASCO in endometrial cancer, the two focus areas that you’re pursuing development in colorectal and ovarian. And then the second question is just on COM503, if you could give us like a rough timeline until this product candidate enters the clinic? That would be appreciated. Thank you.

Okay. Thank you, Mark. I think that I understand what you meant with your question, and I’ll answer, if not, just [quickly answer me again] [ph], send me the question again. So, first, on the endometrial cancer, as we said, we’ll publish the data at ASCO and we gave some insights, this is a small cohort and we’ll be able to show antitumor activity and also safety data from our perspective. As I said in the prepared remarks, this is a way for us to show, again, the potential COM701 in the different indication by the way, an indication that we were predicting through our computational discovery capability to begin with the program. And then later in the year, we will be able to share preliminary findings from the two studies that we’re pursuing now. As I said, CRC is already enrolling with the platinum resistant ovarian cancer study is the screening patient for enrolling, and we will share data towards the end of the year. We aim to complete enrollment of up to 20 patients of the CRC study. So [that on one front] [ph], we may have data from, I don’t believe that it would be the full cohort, but we’ll aim to complete enrollment. And on the ovarian, we aim to complete enrollment of 20 patients out of the 40 in the triplet study, and we share data of whatever we’ll have at that point in time, and then the rest in 2024. And with respect to your question about COM503, IND scheduled for next year.

Okay. Just touching back on the first question, I guess, what I was asking is if we should reasonably expect the lessons or observations from endometrial cancer to directly apply to either colorectal or ovarian cancer?

I think that we look at it, and – Henry, please chime in. I think that we look at it on one hand as indication by indication. So data in one indication is not predictive of success in a different indication. But I think that the totality of the data definitely point to strengthening the view that we have on COM701 that the clinical responses, but also the mechanism of action behind this antibody that we see, that’s very important for us. So that’s my view. Henry, would you like to share anything there on this front?

No. Thank you, Anat. You answered it in general. The thing to remember, Mark, is that, like Anat said, it will be based on indication by indication. One of the things to consider is that for all these indications, the prior therapies are also different, the number of prior therapies are different also. So it’s probably best to look at each indication. So, for example, microsatellite colorectal cancer separates us from endometrial cancer. I think maybe the only thing that’s common to both of these tumor types that they’re microsatellite stable. And that’s one of the commonalities for those two indications. But in general, we’ll have to look at the results separately in order to make a full determination of potential read throughs for the indications that you asked about.

Okay. Got it. Thanks, guys.

The next question is from Stephen Willey of Stifel. Please go ahead.

Yeah, good morning. Thanks for taking the questions. I guess, just with respect to endometrial cancer and ASCO, should we assume that these naïve patients will mostly be IO experienced? And then, in terms of supporting the mechanism of action, can you speak to any biomarker data that you might be able to present? And, I guess, whether or not that’s on treatment biopsies and/or peripheral markers?

I think that on the translational I’ll take it, and then, Henry, you’ll answer about the patient population. I think that on the translational data in general, we’re doing a lot of work and often that not only cover the endometrial, which is, at the end of the day, it’s naïve patient. But on prior studies and also on the current studies that are planned to have extensive biomarker work. We’re harvesting all our capabilities, computational experimental, working with biopsies pretreatment, on treatment, a blood sample own from patients; pretreatment and on treatment few times in order to be able to assess the DNAM axis potential biomarkers and also biomarker discovery that we could do. So we aim to present at a certain point in time, this data probably per indication. We will present very preliminary translational data for endometrial, but I think that biomarker work is still probably towards the end of the year ending 2024. Henry, would you like to discuss the patient population?

Yes, I think it’s only the titles of the abstracts that are currently available now, and so we’ll have to wait to see the details of the presentation for endometrial. And, of course, one of the things that the question you’ve asked will be one of the things that we will be interested in assessing and seeing if contribute to the assessment of antitumor activity. So not just that, but also what will be important is the kinds of therapies that patients have received, also what the performance status of all these patients are, and also what the prior response to some of the therapies that these patients have received in particular for endometrial cancer. So all these parameters including the one that you’ve asked specifically about the things that we will look at and we’ll be able to discuss further once the full abstract are disclosed at the time of the presentation also.

Okay. And then, can you just remind us what the scan frequency is in the two triple cohorts? I guess, I’m just trying to think about the amount of response of valuable patient data that you might be able to show us for the end of this year. Thanks.

Right. So you’re referring to the triplet of COM701, nivolumab and BMS-986207. The scan frequency is every two cycles. So a cycle is 4 weeks, so [every 8 weeks] [ph] for the first 6 months.

Henry, I think this relates to the MSS CRC and the platinum resistant ovarian cancer studies. It’s very interesting. Right, Henry? It’s the same basically.

It’s the same for the MSS CRC, yes.

Okay, great. Thanks for taking my question.

Right. But do remember that for the endometrial cancer cohort that we are going to disclose, it’s also the same scanning frequency, because the legal dose is the schedule is every four weeks, so at the end of every two cycles. Does that make sense? Is it clear?

He passed on. The next question is from Asthika Goonewardene of Truist Securities. Please go ahead.

Hi, good morning and good afternoon. Thanks for taking my question. First, let’s get an idea to report meaningful efficacy data from the CRC and the platinum resistant ovarian cancer cohorts. How much minimum follow-up do you think you will need per patient?

Henry, would you like to address the question?

Asthika, there was a little bit of background, but were you asking specifically for microsatellite stable colorectal cancer?

Yeah, Henry, sorry, that was my little puppy barking in the background there. Yeah, for both CRC as well as platinum resistant ovarian cancer, what do you think the minimum follow-up is that you need per patient to have a good view on what the efficacy is?

I think the minimum follow-up is probably something that’s secondary for those two tumor types you mentioned. What will be important would be what the antitumor activity is. So the earliest benchmark to look at or endpoint will be responsive or durable clinical or disease control rate, right. So stable disease plus special response or plus CR [ph], whatever the case may be in these patient populations, that’s a good benchmark to look at. Remember, this is a Phase 1 study with very few patient population, so that benchmark is probably the most appropriate to look at. The other benchmark to look at would be the depth of responses that we observe in these patient populations, because it’s a small number, sometimes it can be a little bit challenging to interpret the median duration of follow-up you need in a patient population like this. For example, if you have 20 patients that it should be more challenging as opposed to much larger patient population, where you have 95% confident things about that, it will be more conservative.

Okay, so maybe to put another way, Henry, when we see the data that you [asked, later] [ph] this year, we won’t be able to get a good idea of durability of response. It’s really going to be disease control rate and depth of response. That’s going to be – what’s going to be the key to look at the data later this year, right?

Largely the antitumor activity, partial responses, stable disease, and in the unfortunate instance, patients who haven’t responded to this therapies, yes, those are the things I will look at. Because it’s a short period of time, it really will be difficult if you haven’t been able to follow-up on how long those responses are for to be able to disclose the duration of responses. Duration of follow-up also can be challenging, because remember the duration of follow-up includes from the time point patients are enrolled onto the study, until the time that they reach an endpoint for the study either progression or in the opportunity event another hard endpoint like that. So that’s much longer.

Thank you, Henry. I think that’s exactly how we look at it. But I think that I’ll just add that it really depends on the enrollment rate and the more data we will have to share that we think that is meaningful. We’ll try to give as much clarity as possible but needs to take into consideration that even if we enroll the full cohort some of the patients may not be enough time on study treatment and data will be limited.

Got it. Thanks. And I appreciate that. And then just my last question is how confident are you that you will have enough data in hand to see a potential biomarker for both your PVRIG program and your TIGIT program? Thank you.

Maybe I’ll put it in perspective and, Eran, if you want to add, please do so. I’ll put it just in perspective that biomarker work for programs in the field of cancer immunotherapy. I think that all of you understand that it’s not triggered at all in all these fields. If this is not a target that is addressing a specific mutation or a specific target that is for ABC [ph], et cetera. This is really, really hard to come up with. And all the years we ended with PD-L1 and PMDN [ph] anti-high and maybe anti-high. So that’s really hard. I think that the work that we’re doing, which is extensive and is addressing all possible venues on this asset that we’re working on. I think that we increase the chances of success and we feel comfortable to say that we’re doing this work. And when we’ll have data that we think is relevant to disclose, we will disclose it. But I just want to make sure that everyone understands that this is not triggered. If they’re in the biomarker there, I think that Compugen has good chance to identify it. But it’s also given that there will be a biomarker there and, I think, that we’re well equipped to meet the goal if it can be identified. Eran?

Just to add it again, and it’s not mentioned, most people are using PD-L1 as a biomarker, because PD-L1 reflects an immune microenvironment, this is where most checkpoints are working. Luckily, we see responses in PD-L1 negative patients and the biology of PVRIG shows that probably we could tackle these indications, also patients which are immune desert, which are PD-L1 negative. So until now, what we probably quite extensively saw responses in patient were PD-L1 negative. So while we continue to follow PD-L1 for PVRIG combination probably will not PD-L1. And then you have all the usual success, and the non-usual success and we’re doing extensive work sequencing and computationally really trying to identify it. And we do it for maybe a bit related to the question before we do it per indication and across indications. And this is work ongoing with all the challenges that are not mentioned.

Great. Thanks, Anat. Thanks, Henry. And thanks, Eran.

The next question is from Daina Graybosch of SVB Securities. Please go ahead.

Hi, thanks for answering my question. I wonder if you could help us understand more about the partnering conversations or licensing conversations you have going on. I’m interested in specifically what the potential partners are most interested in, which programs, which data points do they emphasize and do you spend the most time on? Thank you.

Thank you, Daina. I’ll relate to this one. While we’re not discussing specifically any partnering discussions that we have or do not have, I’ll try to give some color about the opportunities that we have in the pipeline and how this could be seen. And I think that in general, we are now sitting with a pipeline that is quite rich, that has different partnering opportunities in the form of COM701, COM902, COM503, we also have earlier stage opportunities that are not in the public domain. But we are sitting with unrestricted assets, and they are presenting opportunity in the field of cancer immunotherapy that I believe could bring new treatment options, first-in-class or best-in-class. I think that will COM701, COM902. In COM701, you’re aware of the fact that it is unrestricted since August. I think that for COM701, the real opportunity is what we’re saying for quite a long time that TIGIT/PD-1 will not be enough. And I also related to it in the prepared comments, and companies are now thinking about the agent to combine. We’re saying for quite some time, PVRIG needs to be combined with this in order to enable and in order to allow for the PD-L1 low patient populations or tumor types to respond. We need to deal with the fact that people are judging TIGIT/PD-1 combination based on only TIGIT/PD-1 combination without our third asset, and we have only our own data to show that our third asset is added to it. And hopefully the larger studies will allow us to extend and strengthen this signal. So this is important in terms of how potential external partners may look at it in order to further clarify and extend the DNAM axis hypothesis that we have in general. As we’re showing now in endometrial…

Let me ask one more follow-up then, because you bring it up as your focus is non-dilutive financing in your prepared remarks. How can investors and us have confidence on the timing of that kind of event? Could you talk about maybe certain data points that you think are going to be more important to reach that value? Beyond the attributes of your pipeline, which you will describe, what else can we have in terms of goodness [ph] is happening?

So I think that it’s a fair question, and I think that with respect to COM503, we don’t see any pending will decide to enter into partnership. We don’t see any data points that are making. We have a great package to show exactly what we’re saying about this asset. So that’s one. I think that on the COM701 and COM902, I was saying that it’s a fair question, because I think that it depends on the internal data that we already have. On internal data that we will generate, and it doesn’t mean that we need to get to the end of 2024 in order to be able to share data that is relevant from the internal perspective, but it also depends on external drivers, and it’s not a given – and I don’t think that it’s our goal as well. Definitely this is not our goal to partner everything and stay without a clinical stage pipeline. So we’re putting our priorities in place, and we deal with the internal and external market and with potential discussions. So we believe the assets that we have and as the potential to generate additional cash info for the company in order to support our financial status.

Okay. Thank you.

Thank you.

This concludes the Q&A session. I will now hand over the call to Anat for a final remark. Anat, please go ahead.

Thank you, operator. Before we end the call, I will take this opportunity to remind you of an Investor event we are hosting on Tuesday, May 23, with Drew Pardoll, a pioneer in cancer immunotherapy and a Chairman of Compugen’s Scientific Advisory Board. Drew was the first to propose blockade of PD-1 for cancer immunotherapy, and his research led the clinical development of the first anti-PD-1 antibody. Drew is also a world expert in the DNAM axis. And, I think, you will really enjoy his views on why blocking the 3 pathways in the DNAM axis PVRIG, TIGIT and PD-1 has the potential to generate the next immunotherapies for cancer patients. Thank you for participating today. You may go ahead and disconnect.