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 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, 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 timeline 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, 2023. The company undertakes no obligation to update projections and forward-looking statements in the future. Now, I 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 combination 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. We have the initial clinical and translational data to support our hypothesis. We are the leaders in the unique chemotherapy-free triple combination approach of blocking the 3 genome axis immune checkpoint, PVRIG, TIGIT, and PD-1, and we're 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 patients refractory to anti-PD-1 and in patients whose tumors were immune desert. These data are supported by immune activation that aligns with the COM701 mechanism of action. The goal of the following clinical studies is to strengthen the evidence, help us better understand the contribution of components, and build on the extensive biomarker work to identify the patients most likely to respond. We believe that this strategy provides the fastest route in building a path to registration and de-risk our lead assets, COM701 and COM902 in these two indications. In the first quarter of the year, we executed on our promises. Firstly, we initiated enrollment in or microsatellite colorectal cancer study, and we're excited to be on track to report initial findings by the end of the year, with final data in 2024. At the annual ASCO conference in June, we will present encouraging data showing the preliminary antitumor activity of COM701 in combination with BMS-sensitive TIGIT and ipilimumab in patients with recurrent metastatic microsatellite stable endometrial cancer. This will include data on antitumor activity and safety in nine patients. Patients with advanced microsatellite stable endometrial cancer have limited treatment options. In a similar population of patients, the ipilimumab shows an overall response rate is 10%. The data we will present for our triple combination at ASCO serves as an additional support for COM701-mediated antitumor activity in another tumor type in patients refractory to standard of care. For now, we remain focused on our proof of concept studies in MSS-CRC and platinum-resistant ovarian cancer using our own TIGIT COM902 in combination with our own anti-PVRIG COM701 and pembrolizumab, with a goal to strengthen the evidence in these indications by enlarging the number of patients. However, our data suggests that the treatment potential for COM701 combination goes beyond these two indications. Thirdly, we continue to feed our own pipeline, leveraging our pioneering computational discovery platform. Earlier this month, we gave an oral presentation at CIMT, Europe Cancer Immunotherapy Meeting, on our lead potential first-in-class preclinical asset, COM503, which utilizes a novel approach to harness cytokine biology to potentially treat cancer. We presented preclinical data showing that COM503 binds with high affinity to IL-18 binding protein, freeing endogenous IL-18 and restoring natural killer and T cell activity. We also showed that blocking IL-18 binding protein prevents tumor growth and release IL-18 to activate immunity in the tumor microenvironment without affecting peripheral immunity in murine tumor models. Our approach is unique and different from recombinant cytokines targeting this pathway or from other pathways that were already tested in the clinic. These are given systemically to patients and are associated with safety challenges. The potential advantage of our approach is that our drug, COM503, is an antibody and not a cytokine. This antibody works by freeing the body's own Interleukin-18, where it is mostly upregulated in the tumor microenvironment to stimulate the immune system to fight cancer. Consequently, we believe that it has the potential advantage of avoiding the typical pharmacokinetic and systemic tolerance limitations associated with cytokine administration. Regarding our finances, we have an expected cash runway at least through the end of 2024 to support operations, reach milestones, and de-risk our lead assets, COM701 and COM902. In terms of future funding, non-dilutive funding of our pipeline assets is our priority. We see this as a big opportunity, having three potential first or best-in-class unrestricted assets with the possibility to address a significant unmet need in immuno-oncology. With that, I will hand over to Alberto for the financial update. Thank you, Anat. I'm happy to summarize our financial results. I will start with our cash balance. As of March 31st, 2023, we had approximately $74.3 million in cash compared with approximately $83.7 million as of December 31st, 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 payments 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 payments. To remind you, to date, Compugen received development milestones payments of $2 million, $6 million, and $7.5 million for achieving a preclinical milestones and for dosing the first patient in phase I and phase II studies, respectively. Compugen is entitled to receive an aggregate of up to $200 million in development, regulatory, and commercial milestones for the first products. 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. 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 two 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. If you have a question, please press star one. If you wish to decline from the polling process, please press star two. If you are using speaker equipment, kindly whistle the handset before pressing the numbers. Please stand by while we poll for your questions. The first question is from Mark Breidenbach of Oppenheimer. Please go ahead. Hey, thanks for taking the 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 to the two focus areas that you're think pursuing development in colorectal and ovarian. 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 to quickly answer me again. Send me the question again. First on the endometrial cancer, as we said, we published the data at ASCO, and we gave some insights. This is a small cohort, and we'll be able to show anti-tumor 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 of COM701 in different indication. By the way, an indication that we were predicting through our computational discovery capability to begin with the program. Later in the year, we will be able to share preliminary findings from the two studies that we're pursuing now. As I said, the CRC is already enrolling. The platinum-resistant ovarian cancer study is screening patients for enrolling. We will share data towards the end of the year. We aim to complete enrollment of up to 20 patients of the CRC study. That's on one front. We may have data from... I don't believe that it would be the full cohort, but we'll aim to complete enrollment. 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, the rest in 2024. With respect to your question about, COM503, IV 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 I will look at it, and Henry, please chime in. I think that we look at it as on one hand, as indication by indication. Data in one indication is not predictive of success in a different indication. I think that the totality of the data definitely points to strengthening the view that we have on COM701, the clinical responses, but also the mechanism of action behind this antibody that we see. That's, you know, that's very important for us. That's my view. Henry, would you like to share anything there on this one? No, no. Thank you, Anna. You, you've answered it in general. The thing to remember, Mark, is that, like Anna 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. It's probably best to look at each indication. For example, microsatellite colorectal cancer is a bit fast from endometrial cancer. I think maybe the only thing that's common to both of these tumor types are that they're microsatellite stable. That's one of the commonalities for those two indications. 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've asked about. Okay. Got it. 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 in ASCO, should we assume that these 9 patients will mostly be IO experienced? In terms of supporting the mechanism of action, can you speak to any biomarker data that you might be able to present? 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 that not only covers endometrial, which is, at the end of the day, it's 9 patients, but on prior studies and also on the current studies, that, you know, that are planned to have extensive biomarker work. We're harnessing all our capabilities, computational, experimental, working with biopsies, pre-treatment, on treatment, blood cancer drawn from patients pre-treatment and on treatment a few times in order to be able to assess the genomics, the potential biomarkers, and also biomarker discovery that we could do. We aim to present at a certain point in time, this data, probably per indication, we recognize very preliminary translational data for endometrial, but I think the biomarker work is still probably towards the end of the year and in 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. 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, you know, interested in assessing and seeing if it contributes to the assessment of antitumor activity. 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 the patients are, and also what the prior response to some of the therapies that these patients have received in particular for endometrial cancer. All these parameters, including the one that you asked specifically about, the things that we will look at, and we'll be able to discuss further, once the full abstracts are disclosed, and at the time of the presentation also. Okay. 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 or valuable patient data that you might be able to show us before the end of this year. Thanks. Right. You're referring to the triplet of COM701, nivolumab and BMS-986207. The scan frequency is every two cycles. A cycle is four weeks, so every eight weeks for the first six months. Henry, I think that it relates to the MSKRC and their platinum-resistant ovarian cancer studies, but it's the same, basically. Right, Henry? It's the same frequency. That's correct. For the MSS-CRC, yes. Yes, for the MSS-CRC. Okay, great. Thanks. Take care. Right. Do remember that for the endometrial cancer cohort that we are going to disclose, it's also the same scan, scanning frequency, because the Nivo dose is the schedule is every four weeks. 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 questions. First up, just to get an idea to report meaningful efficacy data from the CRC and the platinum-resistant ovarian cancer cohort. How much minimum follow-up do you think you will need per patient? Henry, would you like to address the question? I think I. There was a little bit of background, but were you asking specifically for microsatellite in colorectal cancer? Yeah, Henry, sorry. That was my little coffee box 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? The minimum follow-up, it's probably something like secondary. For those two tumors, as you mentioned, what will be important will be what the anti-tumor activity is. The earliest benchmark to look at or endpoint will be responses or durable clinical or disease control rate, right? Stable disease, partial response or plus CR, whatever the case may be in this patient population. That's a good benchmark to look at. Remember, this is a phase I study with very few patient population, that benchmark is probably the most appropriate to look at. The other benchmark to look at will 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'll look in a patient population like this. For example, if you have maybe 20 patients, that is a little bit more challenging as opposed to much larger patient population where you have like, 50% confidence intervals that seem to be more conservative. Okay. maybe to put it another way, Henry, when we see this data, that you have this year, we won't be able to get a good idea of duration or durability of response. It's really gonna be the disease control rate and depth of response. That's gonna be what's gonna be the key to look in the data later this year, right? Largely the anti-tumor activity, partial responses, stable disease, and in the unfortunate instance, patients who haven't responded to this therapy, yes, those are the things that we 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 maybe unfortunate event, another hard endpoint like that. That's much longer. I think I'd stick out just, and thank you, Henry. I I think that's exactly, you know, that's exactly what and, how we look at it. I think that I'll just add that it really depends on the enrollment rate. The more data we will have to share that we think that is meaningful, we'll try to give as much clarity as possible. We need to take into consideration that even if we enroll the full cohort, some of the patients may, you know, may not be enough time on study treatment and data will be limited. Got it. Thanks, Anat. Appreciate that. Then just my last question is, how confident are you that you will have enough data in-house, in hand to see a potential biomarker for both your PVRIG programs and your TIGIT programs? Thank you. Maybe I put it in perspective, 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 everybody understands that it's not trivial 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 ADC, et cetera, this is really, really hard to come up with. In all of the years, we ended with what? With PD-L1 and pembrolizumab and MSI-High. That's really hard. I think that the work that we're doing, which is extensive and is addressing all possible avenues on this asset that we're working on, I think that we increase the chances of success. 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'll disclose it. I just want to make sure that everyone understands that this is not trivial. If there is a biomarker there, I think that Compugen has a good chance to identify it. But it's not a given that there will be a biomarker there. I think that we're well equipped to meet the goal if it can be identified. Eran? Yeah. I mean, just to add that again, as Anatt mentioned, most people are using PD-L1 as a biomarker. This is because PD-L1 reflects on immune microenvironments. This is where most checkpoints are working. Luckily, we see responses in PD-L1 negative patients. The biology of PVRIG shows that, probably we could tackle this indication, also patients which are immune desert, which patients which are PD-L1 negative. Until now, and as this occupied, we quite extensively saw responses in patients who are PD-L1 negative. While we continue to follow PD-L1 for PVRIG combination probably will not be the one, then you have all the usual suspects and the non-usual suspects, and we're doing extensive work sequencing and computationally, really trying to identify it. 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 Anat mentioned. Great. Thanks, Anat. Thanks, Henry. 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, Diana. 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. I think that in general, we're 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. We're sitting with unrestricted assets, and they are presenting opportunity in the field of cancer immunotherapy that I believe brings new treatment options, first in class or best in class. I think that for COM701, COM902 and 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 PD-1 will not be enough. I also related to it in the prepared comments. Companies are now thinking about a third agent to combine. We're saying for quite some time, PVRIG needs to be combined with this in order to enable it, in order to allow for the COM701, low patient population, so to want high to respond. We need to deal with the fact that people are judging CDPD one combination based on only CDPD-1 combination without our third asset. We have only our own data to show that our third asset is adequate. Hopefully the larger study will allow us to extend and strengthen this signal. This is important in terms of how potential external partners may look at this and in order to further clarify and extend the BMS's hypothesis that we have in general, as we're showing now in endometrial and additional cancer indications, but also in the specific tumor types that we selected. Focus on in the ovarian cancer and colorectal cancer. That's important for us to pursue, not only in order to speak with the FDA about path forward, but also in potential partnering discussions. That's one thing that is key. I guess that also how CD will perform out there is also important by others and we're looking at it. On the COM503, I'll say that, I think that, you know, I know you're probably aware of it and some are aware of it. There is a renaissance in the field of IL-18 pathway. There is a lot of excitement out there. Small biotech companies are being formed. We're really differentiated on this front, as much as we're differentiated with the platform that we bring to the table. We're addressing this cytokine biology and this pathway in a totally different way than others. We believe that the way that we address it is actually handling the narrow therapeutic window of cytokine. We bring something new to the table and with the excitement that is out there, and it's the right time with the right assets. That's what I can say on the potential partnering discussions. Let me ask a more follow-up then, because you bring it up as your focus, this 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 gonna be more important to reach that value beyond the attributes of your pipeline, which you well described, what else can we have in terms of the confidence of that happening? I think that it's a fair question, and I think that with respect to COM503, we don't see any pending with the time to enter into partnerships. We don't see any data points that are missing. We have a great package to show exactly what we're saying about this asset. That's one. I think that on the COM701 and COM902, I would say 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. It doesn't mean that we need it 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 on external drivers. It's not a given that. 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. That's, you know, we're putting our priorities in place and we're dealing with the internal and external milestones and with potential discussions. We believe that the assets that we have has the potential to generate additional cash inflows 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're hosting on Tuesday, May 23rd, 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. His research led the clinical development of the first anti-PD-1 antibody. Drew is also a world expert in the DNAM axis. I think you will really enjoy his views on why blocking the three 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.