Compugen Ltd Q4 FY2021 Earnings Call

Ladies and gentlemen, thank you for joining us today. Welcome to Compugen's Fourth Quarter and Full Year 2021 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's 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 to present our prepared remarks are Dr. Anat Cohen-Dayag, President and CEO and Ari Krashin, Chief Financial and Operating Officer. For the Q&A session, we will also be joined by Henry Adewoye, Chief Medical Officer and Dr. Eran Ophir, Vice President Research & Drug Discovery. Before we begin, we'd 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 outcomes, the company's discovery platform, anticipated progress, results and timelines for our programs, financial and accounting-related matters, as well as statements regarding our 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 and filed form 20-F filed with the SEC on February 25, 2021. The company undertakes no obligation to update projections and forward-looking statements in the future. With that, I now turn the call over to Anat.

Thank you, Yvonne. Good morning and good afternoon, everyone. And welcome to our fourth quarter and full year 2021 update. I'm proud to say that Compugen made excellent progress in 2021. Our fundamentals have improved and we're delivering on our promises. Compugen has done groundbreaking work on the biology of the key targets of the DNAM axis, PVRIG and TIGIT. This is evidenced by our numerous publications and patent filings. We are pioneers in uncharted territory. We're the first to test in the clinic two agents never combined before primarily focused on PD-1 non-responsive patients. Our differentiated clinical strategy with our potential first-in-class anti-PVRIG antibody, COM701, is to lead the next wave of innovation by executing a unique combination approach to realize the full potential of TIGIT and PVRIG. Immune checkpoint inhibitors have become multibillion-dollar drugs, and are having a major impact on cancer care. However, as most patients do not respond to immunotherapy, there is a need for new drugs for these cancer patients. At Compugen, we believe that immune checkpoint inhibitors that target the DNAM axis have the potential to be a game changer in the treatment of cancer. As we continue as leaders in the DNAM axis by unlocking the potential of both PVRIG and TIGIT pathways with a vision to deliver the next transformational drugs, we're excited to see the growing interest in this phase by major pharma companies providing further validation of our hypothesis and the possibility of opening additional opportunities for us in the future. Data from our clinical studies presented in 2021 with COM701 and COM902 support our hypothesis that treatments targeting the DNAM axis could be effective in inflamed or, even more exciting, less inflamed tumors. Our studies show early signals of anti-tumor activity with immune activation across studies and a good safety profile in mono, dual and triple therapy settings. Today, we would like to update you on our clinical program, upcoming anticipated milestones and report on our financial results for the fourth quarter and full year 2021. I'll start by updating you on our key 2021 accomplishments and 2022 anticipated milestones. Then I will review the clinical program with you. Ari will summarize our financial results, and then I will come back to make a few closing remarks. 2021 has been a year of progress for Compugen with a strong execution across our differentiated clinical strategy. I want to highlight three of our important accomplishments in 2021. First, in keeping with our goals to develop first-in-class or best-in-class immunotherapies for cancer patients who are not responding to currently available therapies, we delivered on our clinical milestones to complete dose escalation studies and begin expansion cohorts across all our programs. These encouraging results from our initial clinical studies reported at major medical and scientific meetings throughout the year pave the way for a comprehensive evaluation of Compugen's DNAM axis hypotheses in our ongoing expansion cohort studies. Second, in keeping with our goal of maximizing value for patients, we expanded our collaboration with Bristol Myers Squibb and are happy to see AstraZeneca progressing their TIGIT/PD-1 bispecific derived from our COM902 into the clinic. In addition, we expanded our research collaborations with Johns Hopkins University. These partnerships support our focus on expediting our early and clinical stage programs and bringing them to the market. Third, in keeping with our leadership position in the field and our goal to advance immune oncology research, throughout 2021, we presented new research and translational data at scientific conferences to support the unique biology of PVRIG and the potential of its blockade to target less inflamed tumor types. In addition, along with one of our trusted advisors and long-term collaborators, Professor Drew Pardoll, we got offered a review on the biology and potential therapeutic relevance of the DNAM axis in cancer immunotherapy in the prestigious high-impact journal Cancer Discovery. Looking ahead to 2022, we're conducting three very important phase 1/2 combination studies. As you know, our clinical strategy has been designed to allow us to systematically evaluate our hypothesis that simultaneously blocking three pathways—PVRIG, TIGIT, and PD-1—in selecting biomarker-informed tumor types may produce game-changing results for cancer patients with inflamed or less inflamed tumors. PVRIG, which is differentiated from TIGIT and PD-1, may be the missing piece when current immunotherapies have failed by potentially generating new ways for T-cells to infiltrate the tumor microenvironment, turning it into a more inflamed environment. Our ongoing combination studies are significant studies evaluating the preliminary anti-tumor activity of COM701 in addition to safety and tolerability in multiple indications. These studies also include a parallel comprehensive translational analysis assessing immune activation to further evaluate our unique drug mechanism of action and potential biomarker identification that may be relevant for future patient selection. Based on establishing proof-of-concept in specific indications, we would share our path forward in such indications targeting the fastest path for registration to maintain our first-mover advantage. Our studies have been designed to efficiently identify the optimal inhibitor combinations and tumor types. Although these are significant studies, this approach, which includes some overlapping indications across studies, is intended to help us understand the contribution of each study drug. Enrollment is underway in our ongoing clinical studies. The first study initiated at the end of June 2021 is designed to evaluate an anti-PVRIG PD-1 combination with COM701 nivolumab in patients with ovarian, endometrial, breast, and microsatellite stable colorectal cancer. The second study, initiated in July 2021, is designed to evaluate the anti-PVRIG PD-1 triple combination with COM701 nivolumab and Bristol Myers Squibb’s anti-TIGIT in patients with ovarian, endometrial, and head and neck squamous cell carcinoma, plus a cohort of subjects who have high expression of PVRL2, which we'll start involving following the assessment of correlation between PVRL2 level of expression and response. The third study most recently initiated in November 2021 is evaluating an anti-PVRIG combination with our wholly-owned COM902, COM701 drug candidates in patients with head and neck squamous cell carcinoma, non-small cell lung cancer, and microsatellite stable colorectal cancer. Our intention is to report data from fully enrolled cohorts of each of these studies, taking into consideration that certain cohorts and indications enroll faster than others, and use the results to define our regulatory strategy on a cohort-by-cohort basis. Based on the current enrollment rate, the first data from combination studies are expected to be reported in Q4 2022, starting with the microsatellite stable colorectal cancer cohorts from the COM701 nivolumab study, and we expect to complete enrollment in all cohorts by the end of 2023. As enrollment progresses, we plan to share further guidance with respect to the other cohorts. Microsatellite stable colorectal cancer is a tumor type that has so far been immunologically unresponsive. There is no approved therapy specifically for MSS-CRC patients, and immune checkpoint inhibitors have demonstrated limited or no activity in this patient population. Treatment in this setting is typically regorafenib or Lonsurf, which show ORR of 1%, median PFS of two months and median OS of 6 to 7 months. As of today, we have presented data from 12 patients using various doses of COM701 with or without nivolumab across studies and have shown encouraging preliminary anti-tumor activity with a disease control rate of 58%, including one partial response of 44 weeks. Our current COM701 nivolumab study consists of an additional 20 MSS-CRC patients, which will help us further assess the potential of this drug combination in this setting. Looking back over 2021, I've been very pleased with encouraging data in our phase 1 studies across mono, dual, and triple therapy in multiple tumor types as presented at ASCO and SITC, as well as the extension of our collaboration with Bristol Myers Squibb based on the data we've presented to date. Three observations from our overall translation data set stand out to me. First, our most recently presented translational data demonstrating immune activation across our COM701 studies with the most potent immune activation in the triple blockade of PVRIG, TIGIT, and PD-1 supports our suggested drug mechanism of action, as well as the differentiation of PVRIG from that of TIGIT and PD-1. Second, I'm pleased with our approach to develop our anti-TIGIT antibody using an IgG4 backbone similar to the leading anti-PD-1 antibodies, with less effective function than IgG1 appearing to be an appropriate strategy. Indeed, in our COM902 dose escalation study, which we presented at SITC, showed that there is no depletion of the CD8+ T-cells, the most effective anti-tumor immune subsets. We were the first to present clinical data with an IgG4 anti-TIGIT antibody with low FC effector function, and we believe this may also come with additional benefits on the safety side to be confirmed in the clinic. Third, our initial data suggested COM701 may have the potential to address less inflamed tumor types, where other new checkpoint inhibitors have not been successful, in line with supporting data from our PVRIG research. In addition, we achieved encouraging signals of anti-tumor activity in our studies with several notable durable responses in heavily pretreated patients who have exhausted all available therapies with a good safety profile. To summarize, our translation and observations, coupled with our encouraging data to date suggest a differentiated profile for COM701 and COM902 with the potential to unlock the value of the DNAM axis as a game changer in the treatment of cancer. I am enthusiastic about our program and look forward to sharing the results of our ongoing studies with you. Before we turn the call over to Ari, I would like to thank the patients and their families, caregivers, investigators, and study sites.

Thank you, Anat. I'm happy to summarize our financial results. I'll start with our cash balance. As of December 31, 2021, we had approximately $118 million in cash compared with approximately $124 million as of December 31, 2020. The company has no debt. Our cash balance reflects Bristol Myers Squibb’s strategic investment of $20 million and $6 million in milestone payments from AstraZeneca received during the fourth quarter. Going into 2022, we expect our cash burn to be in the range of between $44 million to $46 million. Financially disciplined, we are a company targeting our extensive and unique knowledge in this space on specific tumor types and a comprehensive clinical strategy to increase our probability of success of our drugs to help patients. At the current level of operations, we expect current cash will be sufficient to fund our operating plans into 2024. For revenue, we reported no revenue for the fourth quarter of 2021 and $6 million for the year ended December 31, 2021, compared with $2 million for each of the comparable periods in 2020. 2021 revenues are related to the milestone payments from AstraZeneca for those in the first patient in their Phase 1/2 study of the TIGIT bispecific monoclonal antibody derived from our COM902. With respect to R&D, R&D expenses for the fourth quarter and year ended December 31, 2021, were $5.8 million and $28.7 million, respectively, compared with $8.1 million and $22.8 million for the comparable period in 2020. The increase in R&D expenses during 2021 is attributed mainly to higher expenses associated with our various clinical studies, as well as an increase in headcount as we continue to grow our U.S.-based clinical team to support the expansion of our studies. The decrease in the quarterly period is due to a decrease in manufacturing and related expenses. Our G&A expenses for the fourth quarter and year ended December 31, 2021, were $2.7 million and $10.9 million, respectively, compared with approximately $2.7 million and approximately $9.8 million for the comparable period in 2020. The increase is mainly due to increased D&O insurance premium costs that affected the overall industry. During the fourth quarter of 2021, we reported a net loss of $8.6 million, or $0.10 per basic and diluted share, similar to a net loss of $8.6 million, or $0.10 per basic and diluted share in the comparable period of 2020. The net loss for the year ended December 31, 2021, was $34.2 million, or $0.41 per basic and diluted share, compared with a net loss of $29.7 million, or $0.37 per basic and diluted share in the comparable period of 2020. Now, I’ll turn the call back to Anat.

Compugen has done groundbreaking work on the discovery of the PVRIG pathway and the DNAM axis hypotheses, and we're well positioned to maintain our leadership in this new area of cancer immunotherapy. We're actively enrolling in three important combination studies that will guide our registration strategy and we expect to report the first clinical results in Q4 2022. We have a solid balance sheet with a cash balance of $118 million that will support our clinical program and our operations into 2024. I'm very enthusiastic for what's to come for Compugen, and I look forward to updating you on our progress throughout the year. I want to send a special thank you to the amazing team at Compugen, whose dedication has made our remarkable accomplishment possible, and to you all, for joining us today and taking time to follow the company. And with that, we'll now open the call for questions.

The first question is from Stephen Willey of Stifel.

Can you maybe just share with us what your current expectations are regarding efficacy data that will be emerging out of the colorectal cohort by year-end? And I guess what needs to be seen potentially to form a go-forward decision? And then second to that, can you make that decision about going forward before you see combo data from the 701, 902 combo in the same tumor type?

Thank you, Steve, and I'll just refer this question to Henry. I'll just say that in general for all the most of the tumor types that we're addressing, and these are tumor types that are not responsive to checkpoints and their patients do not have many options. So we think that the bar is not very high in terms of numbers. Obviously, this is a very hard-to-treat patient population. I’ll let Henry relate to more specifics.

Thank you very much, Anat, and thanks, Steve, for the question. I want to remind you and everyone listening that these are signal-seeking studies, even though they involve expansion cohorts. We have 20 patients in each of these cohorts that you're referring to. What we're actually looking for is a combination of various factors. Firstly, we are looking for efficacy in terms of a partial response. We are also interested in anti-tumor activity regarding stable disease and the durability of that stable disease. Therefore, it would be premature to start assigning specific numbers that may interest us. That being said, it is worth noting, as Anat mentioned in her prepared comments, that in a particular tumor type, seeing a patient with a partial response, such as in colorectal cancer, who remains on treatment for 44 weeks is significant. This is significant for several reasons, one being that this tumor type usually does not respond well to immune checkpoints, as their activity is very limited. This alone indicates that we have a signal, which is more important. Additionally, as disclosed at ASCO last year, the quality of the patients enrolled in the colorectal cancer cohort is also important. Of the 12 patients we enrolled, some have exceeded the typical median progression-free survival for this patient cohort, as noted in our summary plot. These are the various parameters we are interested in, and we will continue to include results from all other cohorts to make a more informed judgment regarding anti-tumor activity and the next steps for Compugen.

Stephen, I’ll just add one more thing that relates not only to the clinical data, but also, as you know, we have a comprehensive translational program that we apply to all the different studies on all the cohorts. We really look at the translational data as a very important parameter. This will be taken into consideration as well. For the COM701 and COM902 combination, the data is from open studies, and we see the data. So this is definitely a parameter we will take into account.

And then maybe just lastly is the year-end '23 guidance that you're providing here for completing enrollment in all cohorts. Is that in any way rate limited by the diagnostic work that you're doing to establish PVRL2 expression for enrollment into the basket cohort?

That's not limited, the program is ongoing. We're doing a lot of work in order to make sure that we have the samples and then we can test the expression profiles of the DNAM axis members, specifically PVRL2. So at the time that we feel that we have enough in order to correlate expression to response, we will start the basket study.

The next question is from Reni Benjamin of JMP Securities.

I guess just starting off, the timing for the dose expansion studies has kind of thrown me off a little bit. Can you just give me a sense as to what are the factors that are leading you to think that enrollment would only be complete by the end of 2023? I always assumed that once the dose expansion was done, that the expansion studies would enroll a lot quicker, so if you can give us a sense of that and then I have a follow-up.

Sure. Basically, there are two parameters. The enrollment rate that is very different for different indications and CRC by nature is more prevalent, less rare treatment, so it is enrolled faster. There are indications that are harder to enroll, and the pace is slower. So this is one parameter. And also I want to remind everyone, through these significant studies, we have 20 patients per cohort, but we have many cohorts and many studies ongoing. So the total number of patients that we're enrolling is very large. So it is important for us to make sure that we do this analysis of the DNAM axis in a way where we maximize the opportunities, and that we maintain the leadership in evaluating this axis and also to make sure that these are not only significant studies, so we can really relate to the contribution of components. But let's make sure that we remember that these are not small studies, and we're really enrolling faster, we're on execution. And we restart sharing data in Q4, and these studies will continue to enroll, and we will continue to share guidance and data, but that's the two parameters: the enrollment and the size of the studies.

And just as I think about news flow, have a sense of obviously, how the news flow from the company is coming out. Could you talk a little bit about maybe your partnership programs, and any sort of a sense as to when we might see news flow from those programs? And I understand, these are partner programs; you might not have as much control or insight into that. I guess just related, you have an early pipeline, I think you have some myeloid candidates and the like, can you give us an update as to how those might be progressing, and when we might see an IND for a new agent?

Certainly. Regarding the partner programs, we have the AstraZeneca program, which is a bispecific derived from our COM902, specifically a TIGIT/PD-1 bispecific. This program has recently commenced clinical trials. The progress of this program is primarily tied to our partners, and the sharing of information depends on them. We can't provide specifics, but they are making progress. As for the Bayer program, the last update we provided indicated that it is being tested alongside their KEYTRUDA. Bayer is focusing on first-line IO naïve head and neck squamous cell carcinoma. Again, the progress relies on Bayer, and they control the communication regarding it, but this program is also advancing. Concerning our early-stage pipeline, we haven't shared details about it, aligning with the reasons we've previously stated for not discussing it publicly. We are concentrating on several programs guided by our computational discovery capabilities. We are not a "me too" company; our aim is to modulate immune-suppressive cells in the tumor microenvironment. We will disclose information about these programs based on their development stage and the competitive landscape. It's similar to what happened with PVRIG; once we disclosed information, the competition clock started ticking. We have noted the validation of the various competitions on new targets that we have identified, but we also want to ensure that the stages of development allow us to maintain our leadership position.

The next question is from Mark Breidenbach of Oppenheimer.

This is Jacqueline for Mark from Oppenheimer. Thanks for taking our questions. My first question is, are you taking any steps to limit the number of prior therapies for patients enrolling in the expansion cohort versus what we saw in the all-comers study population at the SITC conference?

Henry, I guess you'll address that one.

We are not limiting the number of prior therapies for patients. What we're actively doing is collaborating with investigators to ensure that enrolled patients meet all eligibility criteria for the specific studies. Additionally, we are making sure that these patients have received the appropriate therapies before joining the study, and we review each patient with the investigators very frequently. According to FDA guidance for Phase 1 studies, patients must have exhausted all available standard-of-care therapies before being enrolled. This can vary depending on the tumor type and previous therapies. As standards of care evolve, such as in endometrial cancer where patients now receive lenvatinib and pembrolizumab, we encourage investigators to consider our clinical trials once patients have exhausted those therapies. Our goal is to offer patients the chance to enroll in our trials earlier, before they receive other investigational agents. This approach applies to studies like COM902 and the triplet study with COM701 and pembrolizumab, highlighting our ongoing engagement with investigators.

And my second question is R&D expenses were chopping down in 4Q. How should we think about modeling going forward in 2022?

We had a slight reduction in the fourth quarter, it's mostly shifting between quarters, it's a good question. And basically going forward, you should assume that the run rate would be more similar to the third quarter, which was roughly $8 million or $9 million and that's fairly what you're going to see in 2022 as well.

That's it for me. Thank you for taking my questions.

Thank you.

The next question is from Tony Butler of ROTH Capital.

I have a couple of questions. Can you clarify how you are defining high in relation to the basket trial with PVRL2? I also have two follow-ups.

So yes, Tony, thank you. This is exactly what we do now. So we need to explore what does it mean high and low for enrollment. And this is defined in correlation with anti-tumor activity. So we're now evaluating the expression levels as compared to response in all the studies that we have, and when we will set the threshold, we will then initiate enrolling for the basket study. So this is still not being enrolled.

In the doublet for non-small cell lung cancer, it’s interesting to enroll the cohort and treat them with the double, assuming they have failed prior PD-1 therapy, but I’m curious why it may not also be included in the triplet. Additionally, do you think that anti-PD-1, particularly in combination with anti-TIGIT and anti-PVRIG, leads to increased exhaustion for T-cells? In other words, do they no longer exhibit CD8 and CD28 positivity?

So, I would relate to the triplet first and/or maybe as you eluded from the doublet of the COM701, COM902, there is an PD-1 three regimen. For the triplet, we focused on the triplets on tumor types that are not responsive to PD-1 inhibition other than the head and neck that is more inflamed compared to the other indications that we have. We limited the study. It does not mean that we will not expand triplet assessment in non-small cell lung cancer but at this point in time we're not assessing non-small cell lung cancer in the triplet. Later on related to the triplet or blocking with the free pathways with respect to driving increased exhaustion. Eran?

Yes, overall, PD-1, like many other checkpoints, is helping to rejuvenate exhausted cells. PVRIG also targets exhausted cells similarly to other checkpoints. What’s noteworthy is that PVRIG shows more pronounced expression during earlier differentiation, and these cells typically possess a larger indiscernible space. By blocking PVRIG, we may start to observe clear early signals in clinical trials, which can improve the interaction between less exhausted early memory cells and dendritic cells. This may lead to additional pathways for effector cells as we navigate the microenvironment. At this stage, the cells are likely to show triple expression of PVRIG and PD-1, and the triple blockade might be significant, or in some cases, a specific combination of two may also be impactful. In summary, I believe that PVRIG could provide a complementary treatment alongside TIGIT and PD-1 or potentially offer options even in the absence of PD-1 for patients who typically do not respond to checkpoints, due to this distinct expression profile, revealing a truly clinical biological relevance.

Last question is around abscopal effects, especially in CRC? I don't know and I don't think this has been addressed. But were any of the patient stage 4 cohort of cancer patients is previously treated importantly to assuming then by definition, they have liver mets? Has it been determined at all or observed that those mets also were in fact stable and/or were maybe part of that partial response patient that was observed in the previous cohorts of CRC patients?

Henry?

I cannot provide specific patient details, but I can clarify how assessments are conducted, which should help answer your question. It's important to remember that when evaluating responses in our studies, especially in colorectal cancer, we use resist version 1.1. This involves looking at patients in the expansion cohort who have target lesions. All patients enrolled in the colorectal cancer cohorts are defined by their disease, which can manifest in the liver, lungs, or other areas. These target lesions are factored into the assessments. We've noted that investigators have chosen some stagnations in the liver or lungs for measurement and monitoring. These observations influence how patient responses are reported, like stable disease, which indicates there hasn't been a significant increase in the size of target lesions. We also noted cases of partial response in patients with microsatellite stable colorectal cancer, as well as cases of progression. The assessment method includes reviewing some non-target lesions for any potential subjective increases. Thus, while we cannot discount the possibility of the abscopal effect, we are employing refined and established criteria for evaluating responses in these patients.

Maybe just to add in this regard and actually linking this to the previous comment about the PVRIG expression on every memory cell. So we have recently actually presented the industrial pre-patient to responding clinically. We followed up that in non-treating biopsy taken from liver metastasis, which is normally an immunosuppressive environment and we have seen a dramatic immune modulation; we have presented that in the last SITC summit. So we see actually huge increase of an influx of new multi-cell clones penetrating that specific lesion in the liver. And we saw increasing tolerability, increasing immune activation. And this is one of the observations I mentioned, preliminary observation that supports, especially in this indication that normally you wouldn't expect to see this kind of modulation in liver alone. So this is very encouraging to see such a new modulation and increasing infiltration in such liver patients.

The next question is from Daina Graybosch from SVB Leerink.

I'm going to make a statement that I've been thinking about, and I think a lot of the questions are thinking about, you're enrolling a lot of patients, approximately 220. And I think our worry is collectively, that you've set the ambition bar so high, because of your belief and being able to have PVRIG stimulate an immune response. And it's harder to treat patient populations, whether it’d be like colorectal or ovarian, or in lung after they've exhausted other IO treatment. So I think the risk that I and I think a lot of us are considering is could you have a good hypothesis and a good treatment, but then you enroll all these patients, and we still fail to see a really strong signal because the threshold is so high? And I wonder, as you look at that, can you point to any cohort or combination where you think the threshold is not so high, that we are more likely to see a signal? And I'll make an example like with TIGIT, these cohorts had been a role for TIGIT? I don't think we'd be where we are with TIGIT today. We're excited about TIGIT, because Roche’s Genentech did a frontline study, which they could, because they were combining on top of standard-of-care, in which you guys also have standard-of-care Opdivo that you could do a strategy like that with the combinations that include Opdivo but have chosen not to. So just I’d love for you to react to that statement and tell us all where we could have some optimism that you haven't set the threshold too high.

Thank you, Daina. That's a very good question. We chose to focus on the non-responsive patient population, specifically those with less inflamed tumor types and PD-1 non-responders, based on the groundbreaking science we have. That is indeed our plan. While we do have more inflamed tumor types in areas like head and neck cancers, our main focus is on less inflamed tumors. In head and neck, we also have an IO naïve arm, but the aim is to target the less inflamed tumors. As we progress, we are keeping all options open, including pursuing inflamed tumor types. It was crucial for us to address the potential advantages PVRIG may provide, even though it carries higher risk. As a company, we are evaluating various strategies to mitigate that risk, and we are considering all options available to us.

This concludes our Q&A session. I will now turn the call back to Compugen's President and CEO, Dr. Cohen-Dayag. Would you like to make a concluding statement?

Yes. Thank you, operator. Thank you for joining us today and your continued support. Stay safe and healthy.

Thank you. This concludes the Compugen Ltd. fourth quarter 2021 financial results conference call. Thank you for your participation. You may go ahead and disconnect.