Good morning, and thank you for joining us at the 3rd day of the Needham Healthcare Conference. My name is Gil Blum, and I'm a senior biotech analyst here at Needham & Company, covering the immuno-oncology and gene therapy subsectors. It is my pleasure to have with me today Anat Cohen-Dayag, the President and CEO of Compugen. And without further ado, please go ahead. Thank you for everyone that is listening to us today, and thank you, Gil and the Needham team, for inviting us for presenting the Compugen opportunity today. For those of you that are not familiar with the company, Compugen is a clinical stage cancer immunotherapy company. We are pioneers in computational target discovery, and this is an area that is getting more traction today, an exciting area due to the AI revolution in drug discovery. Along with our computational discovery platform, which is the powering engine behind our competitive edge as a company and behind our diversified portfolio in the future portfolio. There is also another attractive aspect for the company. This is the fully owned clinical programs, the multiple fully owned clinical programs, the multiple validating strategic partnerships that we have. The early stage, the multiple programs in the early stage pipeline that we have. The 3rd attractive aspect of the company is the solid balance sheet, which is expected to take us into 2027. This is including the $60 million that we received from the Gilead collaboration around the COM543, a preclinical stage licensing deal. An upfront payment. It's including the $10 million received from AstraZeneca for the first patient dosing of the Phase III study that initiated last year. It is also taking into consideration additional $30 million that are expected to be received from Gilead upon IND clearance, which is expected to happen this year. Partnering is a key component of our strategy, and we're focusing on collaborating in order to extend the reach of our innovative drugs to patients, to cancer patients. In general, this is an exciting time for Compugen. We have the fundamentals in place in order to be able to hopefully realize the value of our drugs. So with that, we move, we move forward. I think that all of you are familiar with the TIGIT space, TIGIT being a drug target that is being now evaluated by multiple pharma companies in a broad manner, in multiple indications and patient populations. And there are Phase II randomized studies that are actually showing that there is a benefit of adding TIGIT to TIGIT PD-1 blockade. However, the activity is limited, and we Compugen were stating it over and over again. And that was mainly when we discovered PVRIG as a 3rd pathway that is intersecting with TIGIT PD-1 pathways through DNAM. So basically, this is a story of 3 pathways that are intersecting, and we were always saying, and we still say that. That while TIGIT blockade together with PD-1 is active in certain indication and in certain patient populations, it is not going to be enough in other cases, and there is another missing piece, another pathway that should be inhibited in order to maximize the response. We believe that this is PVRIG due to the biology and the potential synergy that we were showing in preclinical studies, and now also in clinical studies. We believe that PVRIG can add to the blockade of TIGIT PD-1 in overcoming resistance to cancer immunotherapy drugs. This is based on what we discovered as the biological rationale for targeting PVRIG. We first discovered PVRIG. We were unlocking the biology. And eventually what we've found is that while PVRIG is acting like other checkpoints, as you can see in the right side of the slide, in reinvigorating the exhausted cancer fighting T cells in the tumor microenvironment. In the left side of the slide, what we've discovered is that PVRIG expressed in stem cell-like memory T cells. And that its ligand, PVRL2, is expressed on dendritic cells. The expression on these two cells suggests that it has a role in recruiting additional cancer fighting T cells and expanding them within the tumor microenvironment. Therefore, blocking PVRIG may sensitize the tumor microenvironment to respond to PD-1 and TIGIT blockade, and thereby avoiding resistance to cancer immunotherapies. We are the first to move ahead with the PVRIG blockade. COM701 is the most advanced program in targeting PVRIG in the industry, and there is increasing competition with time, with multiple companies, including GSK, in the front. We've tested in Phase I studies COM701 across multiple indications, and we were able to show that COM701 as monotherapy. And also in combination with TIGIT PD-1, mediating clinical benefit across multiple tumors. Typically not responding to immunotherapy, actually proving what we were finding biologically. Not only responding in tumor types that are typically not reactive to cancer immunotherapy, but these are durable responses. And with a good safety profile. The tumor microenvironment of this responding patient population is also undergoing modulation. That is in favor with the mechanism of action of PVRIG blockade of COM701, which is actually increased infiltration and proliferation of cancer fighting T cells within the tumor microenvironment. And you can see here. This is the COM701 driven mechanism of action. This is a patient that is having partial response for over 18 months. Treated with COM701 monotherapy. What you can see here is that a biopsy of a patient taken pre-treatment was actually PD-L1 negative, a complete desert. This patient had a surge of interferon gamma that is associated with immune modulation. Just ahead of the response of the partial response that it was presenting for a long time. And this is actually a point that we were taking initially when we saw it as very much in line with the mechanism of action of PVRIG blockade. Turning cold tumors into more inflamed tumors, enabling the response to PD-1 and TIGIT blockade. In platinum resistant ovarian cancer patients, we were seeing a 20% overall response rate. And that was in this patient population that was responding. We were seeing patients that were responded durably with over 16 months of response and with a favorable safety profile. This is not a given. First, this is encouraging as compared to the standard of care. The median duration of response in standard of care single agent chemo is 3-4 months, and with ADCs is about 7 months. So that was encouraging. But also what was encouraging for us is the reaction of the investigators that started to see these durable responses, the stabilization of disease over time, and all of this in patients that were exhausting all treatment options and in patients that they were seeing an increased quality of life. And that's not a given. The safety profile of this combination is favorable. We were also seeing in platinum resistant ovarian cancer some indications for PVRL2, the ligand of PVRIG, serving as a potential biomarker for patient selection. We started to see some correlation between the levels of PVRL2 expression and clinical benefit. And with this, I can say that in the which you know, which this is the biomarker data that we have is really in conjunction with the overall response rate and the durability of response. It's generating some edge in platinum resistant ovarian cancer and pointing to a path forward in this indication for the company. Today we're having an ongoing study in platinum resistant ovarian cancer designed to increase the number of patients being treated in triple combination therapy of PVRIG, TIGIT, and PD-1 blockade. And the idea is that if the data will repeat itself biomarker wise and also the overall response rate and durability. It opens the door for us to go ahead with a biomarker enrichment strategy as a path forward for potential registration studies. Another cohort in MSS-CRC, a cold tumor type. We were able to show in 22 patients cohort a 12% overall response rate. And here in this case, in patients with liver metastasis. This is significant because 70% of the patient populations in this line of treatment is having liver mets. And these patients are historically not responding to drugs. Currently, the standard of care for this line of treatment, 3rd line in m-MSS-CRC, is actually Lonsurf and Bev. And it is presenting 6% overall response rate across the patient population. About 70% disease control rate, which is actually the one parameter that is correlating with the median overall response and with the median overall survival of more than 10 months. Following on this data, we've initiated a study in additional cohort of MSS-CRC being treated with triplet combination of PVRIG, TIGIT, PD-1 blockade. It is designed to add on the data that we've generated for the doublet of COM701 plus PD-1 inhibition. The idea is to be able to see if we have a competitive edge in this 70% of this patient population of patients with liver mets across the overall patient population. Even though it's a single arm study, small numbers, we will also look at the median overall survival rate of this patient population in order to better understand on top of overall survival and disease control on top of overall response rate and disease control rate whether we have an edge in MSS-CRC. And also here in MSS-CRC, we were seeing extensive tumor microenvironment modulations of patients that were responsive specifically. What you see here are the two responders that are having liver mets. They started in the left side of the slide. You can see they started as almost complete desert in terms of cancer fighting T cells. And they were undergoing infiltration of T cells and expansion of the T cell population upon response. And that's again supporting a COM701 driven mechanism of action. On top of the data that we're seeing in a monotherapy. Now moving to our strategic collaborations. I'll start with AstraZeneca. And our partner AstraZeneca is developing rilvegostomig. This is a PD-1/TIGIT bispecific antibody where the TIGIT component is derived from our own COM902, our own TIGIT antibody. AstraZeneca initiated a Phase III study in biliary tract end of last year. From our perspective, it brings us closer to having an opportunity for a marketed drug. The fact that they are testing this asset, rilvegostomig, in a broad clinical strategy across multiple indications, lines of treatment, different combinations actually increases our probability of getting access to additional milestone payments and future royalties. And moving to Gilead, this is the recent collaboration that we entered end of last year, a preclinical stage license agreement with a deal value of up to $848 million, including $60 million upfront payment and $30 million in near-term milestone payments, and with single-digit to low double-digit tiered royalties on net sales. This collaboration under this partnership, we're taking this asset COM543 into Phase I studies. And I believe that the fact that we've entered into this collaboration and are taking this asset forward. is really pointing to the strength of Compugen in discovery, research, and development. COM543 is a potential first-in-class anti-IL-18 binding protein antibody. It is a new way that Compugen identified to harness cytokine biology, specifically in the IL-18 pathway, and targeting for cancer for targeting it for cancer with an antibody. And this is very different from trying to turn a cytokine into a drug. And using an antibody is actually preventing, having the potential to prevent the challenges that are presented by cytokines. This deal that we've entered with Gilead is actually highlighting the potential of COM543 differentiated approach to harness cytokine biology. And it is strengthening our balance sheet. And this is a way for us to take the cash that we have and allow ourselves to enhance our diversified portfolio, to enhance our discovery capabilities, and to make sure that we also advance. Not only our clinical stage programs, but also the multiple early stage programs being able to come up with the next COM 543 opportunity. Moving into what's next. 2024 is supposed to be a catalyst-rich year for Compugen. We're expected to have multiple data readouts with our diversified portfolio. First, with the 2 clinical stage assets, COM 701, COM 902, we are conducting 2 proof of concept studies. They are testing these assets with PD-1 inhibition in MSS-CRC, as I described, and the data will be available this quarter. And in platinum resistant ovarian cancer, as I described, and the data is expected to be available in Q4. We're on track with our COM 543 program, planning to submit IND in the second half of this year, and with a plan to initiate the Phase I study following IND acceptance. With the AstraZeneca partnership, AstraZeneca is expecting to have data on 2 studies this year. One study is the GEMINI hepatobiliary Phase II GEMINI study in hepatobiliary cancer. And to remind you, they initiated already the Phase III study. And also the ARTEMIDE-01 study in hepatocellular cancer in the frontline setting. And as I said, it's exciting times for it's exciting time for Compugen. We do have the fundamentals in order to be successful. And we are moving forward aggressively with execution. And with that, Gil, I'm happy to take questions. Thank you, Anat. Maybe, maybe a good place to start. So, your results appear to have, you know, some patients who have long-lasting responses. Will we have a median PFS assessments from some of these studies? So for the colorectal cancer patients, which is a study that started prior to the initiation of the platinum resistant ovarian cancer. We believe that we will be able to gain insight around the 12 months overall survival rate. And as I said, even though it is a single arm study, small study with these caveats. We will be able to look and understand whether we have an edge, taking into consideration the rest of the parameters: disease control rate and overall response rate, and understand whether we have an edge across the population. And in the liver mets population. From a development standpoint, has a company considered combining some of your agents with cytotoxic agents as well? This is a known strategy in immune oncology, more in the front line setting. It's a very good question. So, we're following now at this stage. What we believe is a way to really maximize the response when you're combining immune oncology agents. In really releasing the blockade of 3 pathways that are intersecting. We believe that blocking only these 2 is really missing, and the missing piece is PVRIG, and you need to do that. And our data is suggesting that in tumor types that are not responsive to PD-1 this is possible. The data that we see is COM701 driven. And this is data that you don't see with PD-1 inhibition in these tumor types. That's one path. But in general, we do recognize that the combination between immune oncology agents and cytotoxic agents makes sense. The reason for this is that the cytotoxic agents is kind of priming the tumor microenvironment. And then with immune oncology drug, you can extend and prolong the response that is usually. Shorter term with cytotoxic agents. We believe that in certain indications, in some of them that we're already pursuing. There starts to be some data with cytotoxic agents. And obviously, when we will pick our path forward into a registration path within an indication. We will take it into consideration. I do have a question about the specific biomarkers. So you mentioned PVRL2. PVRL2. Yeah, PVRL2. Yeah, PVRL2. Yeah, PVRL2. Nectins are complicated, right? There's a lot of nectins that signal simultaneously. Is there a chance that there is additional, you know, important biomarkers that may be required as part of this pathway? For example, PVR. So. I relate to PVR in a minute, but first I'll say, you know, never say never. I've learned along the years. I think we've all learned the biology is complex, and sometimes you don't know what you don't know. I will not say not at all. But I will say, and I will relate to PVRL2. As part of COM701. PVRL2 as a biomarker for COM701 response. COM701 combinations response. We believe that we were looking very carefully on the different DNAM-1 axis components, the receptors and the ligands. And at this point in time, we believe that the one protein that is found in a correlation, and I'll say that again, it's initial correlation. Small number of patients, we'll still. This is work that we're doing now in the platinum resistant ovarian cancer cohort to verify the data and to extend the dynamic range of the assay in order to be able to select a cutoff. We believe. That's the finding, and so at this point in time for other DNAM-1 axis members, I'll say no. But you know, we're staying open, and as a company that is an expert in discovery. I believe that we have the computational capabilities and the experimental capabilities to come up with anything else if it's there. And another question of biology, and this is kind of looking across your patients, not just the responders. Have you seen an increase in PD-1 expression, regardless of response? It's a very good question, and I'll say. If you think here first, from the mechanism of action of COM701. In general. That is actually. We think have a role in the recruitment and the expansion of these T cells, the cancer fighting T cells in the tumor microenvironment. There is an increase in PD-L1 levels in general. That's the mechanism that it is acting there. Thereby we think that it is sensitizing the tumors to respond to PD-1. But But we see it also in stabilization of disease. So it is not really the response per se. Sometimes not only in stabilization of disease of over six months, which we consider as a clinical benefit, sometimes in stabilization of disease that is shorter than that. And in few cases also where you don't see the response. But we believe that this is more of a threshold. Like you need to pass a certain threshold in order to be able to start to get a response. You need to sensitize the tumor microenvironment to a certain extent, probably in order to see a response. Let me just clarify kind of what I'm getting at. So I'm trying to understand how universal of an effect it is, meaning if it works broadly in any, you know, patient. So if T cells would enter the tumor microenvironment, and by entering the tumor microenvironment, PD-L1 expression would increase, right? So that's that would be indicative of a broad effect, regardless of what tumor type you're talking about, and that's just, I think, an interesting finding. True. I will say, but I will add, and sorry, but I will add that PD-L1 is not a biomarker that is predictive for COM701 response. It is not. We've tested it. It is not at all. Okay, and kind of a last one, and this is broader for the space and more general. What. What do you think is gonna be a main driver here? I mean, most investors have moved on from TIGIT. What what shakes this up? That's a very good question. And yes, and there are investors that move away from TIGIT. I think that as long as pharma is testing it broadly, the jury is still out. I do think, as I said in the beginning, that the Phase III randomized studies are pointing to an effect. There is an effect. And the question is, what will be the Phase III data? So obviously the first data that at least we know we know publicly that is that may happen is the Skyscraper-01 data from Roche/Genentech that is anticipated in the second half of the year. And it is, if if it is not for this one, then it's Merck. Gilead. AstraZeneca. All of them are conducting Phase III studies. I think that Merck and Gilead are having multiple Phase III studies. I guess that the readouts will be there in later than 2024. Probably 2025, and maybe later. So it may take time. It may take time. I think that the first time that there will be Phase III data, and it will be a point where there will be some insights into what's going on with TIGIT. Okay. Alright. Thank you, Anat, for taking the time today. Gil, thank you very much.