Compugen Ltd Q2 FY2022 Earnings Call

Ladies and gentlemen, thank you for joining us today. Welcome to Compugen's Second Quarter 2022 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, Joni, and thank you all for joining us on the call today. Joining me to present prepared remarks are Dr. Anat Cohen-Dayag, President and Chief Executive Officer; 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 potential 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 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. With this, I now turn the call over to Anat.

Thank you, Yvonne. Good morning, and good afternoon, everyone, and welcome to our second quarter 2022 update. Today's call will focus on the strategic decision we have taken to move the company forward with an anticipated extended cash runway through the end of 2024. I'm happy to say that we continue to execute on all fronts and have made significant progress. We now have sufficient insight to focus on two prioritized indications and wind down the existing cohort expansion studies in our current Phase 1 program. Our focused development plan, resulting from the strategic decision to wind down these studies, results in the conclusion of our collaboration with Bristol Myers Squibb. I would like to thank them for our productive interaction and for supplying nivolumab and their anti-TIGIT antibody for our Phase 1 program, enabling us to initiate the triple and dual combination studies to evaluate our DNAM-1 axis hypothesis at a time when our own differentiated anti-TIGIT, COM902, had not yet reached the clinic. I would also like to thank all the investigators, TIGIT staff, and patients who participated in our studies to date. I believe that our strategic decision to move forward and prioritize two indications while ending the current Phase 1 studies is the right thing to do at this time. With Compugen, I believe that it is the optimal path forward for our company. We believe that this decision will enable faster value creation for our stakeholders and reflect better use of our current resources for the benefit of patients for the following reasons. First, it gives us flexibility and allows us to be nimble and move quickly and efficiently to focus on two prioritized indications that we believe offer the highest probability of success and may support the future path to registration. Second, under these market conditions, it reduces the risk posed by further broad assessment of three large parallel studies in hard-to-treat immune checkpoint inhibitor-insensitive indications with patients who have exhausted all treatment options. Third, it extends our cash runway through the end of 2024. Fourth, it enables us to leverage the combination of our own in-house clinical stage potentially first-in-class anti-PVRIG antibody COM701 and to switch to and develop our differentiated anti-TIGIT antibody COM902. And finally, it gives us the flexibility and the greatest opportunity to advance and partner our clinical assets and support a future path to registration. I'm excited about what we have achieved and what we can achieve, and I look forward to focusing on execution and delivering value. During today's call, I will reiterate the belief we have in our already stated differentiated clinical strategy, provide direction behind our strategic decision to conclude our current Phase 1 program early, our choice of prioritized indications, and the path forward. I will also briefly touch on advancements in our preclinical pipeline. Ari will then review second quarter financials, and I will close with a few remarks. Starting with our differentiated clinical strategy. Compugen has done groundbreaking work to identify and develop two proprietary novel immune checkpoint inhibitors that have the potential to be first-in-class and best-in-class, COM701, an anti-PVRIG monoclonal antibody, and COM902, an anticipated monoclonal antibody. As a company with vast experience in these pathways, our narrative remains the same. We have a differentiated clinical strategy in uncharted territory supported by strong signs. Compugen is the only company studying the triple blockade of the DNAM axis targeting PVRIG, TIGIT, and PD-1 in the clinic. We are leading the way, and others are following. We recognize that targeting TIGIT is a competitive space, with the most advanced programs already being evaluated by Pharma in Phase 3 studies. This is a testament to the promise of modulating this pathway to enhance anti-tumor immune responses. Importantly, we believe that not all TIGIT antibodies are the same. We're the first company to present clinical data with an IgG4 anti-TIGIT antibody with low FC effector function, and we have good reason to believe this is the right design to pursue. In contrast to others, we have shown clinically that COM902 avoids depletion of CD8+ T-cells, the cells important for anti-tumor activity. We believe the IgG4 backbone may come with additional safety benefits to be confirmed in the clinic. We have also stated that blocking only part of this axis may not be enough. Based on our groundbreaking science demonstrating unique value for PVRIG versus other checkpoint inhibitors, and the early clinical and translational data we have presented to date, we believe targeting PVRIG may be the missing piece by creating a more inflamed environment. In our COM701 monotherapy and combination with nivolumab studies presented at ASCO in 2021, we showed partial responses or stable durable disease in patients with low expression of PD-L1, with tumors that are less inflamed and generally less responsive to approved checkpoint inhibitors. In addition, we showed that triple combination treatment was associated with potent immune activation greater than what was seen with mono or dual therapy. Next, moving to our strategic decision to advance two prioritized indications and end our Phase 1 cohort expansion studies. Our Phase 1 cohort expansion program was designed to allow us to systematically evaluate our hypothesis that simultaneously blocking three pathways: PVRIG, TIGIT, and PD-1 in selected tumor types could extend the reach of cancer immunotherapy. We also included studies testing subsets of these three pathways by blocking only two pathways and pursued these studies in overlapping indications with the intention to learn as much as possible about the dominance of the various pathways and the contribution of components in the hardest-to-treat tumor types. In selected tumor types, we identified initial signals of anti-tumor activity and insights into the contribution of components in overlapping indications. In cases where part of the translational work has been performed, we were able to detect immune activation, suggesting a COM701 mediated mechanism of action. We believe the initial signals of anti-tumor activity that were seen with COM701, coupled with changes occurring in the tumor microenvironment in some of the hard-to-treat, checkpoint non-responsive indications, support further evaluation with COM701. To this end, we have decided to move on independently and with more flexibility with two prioritized indications, which we believe offer a higher probability of success and may support the future path to registration. One, in a less inflamed tumor, microsatellite stable colorectal cancer, with a low bar to be compared to standard of care, but a tumor type that reflects a higher risk as it has so far been immunologically unresponsive. The second is an inflamed tumor non-small cell lung cancer in anti-PD-1 treated patients. These tumor types are more immunologically responsive and therefore may present a more permissive environment for DNAM axis activity, although the patient population is challenging to treat. Going back to microsatellite stable colorectal cancer. There are no approved therapies specifically for this patient population, and immune checkpoint inhibitors have demonstrated limited or no activity in this patient population. Treatment in a third line or greater setting is typically regorafenib or Lonsurf, which show an overall response rate of 1% median progression-free survival of two months and median overall survival of six months to seven months. Also note, pembrolizumab monotherapy has shown a 0% response in this population, improving only to an overall response rate of 6% in combination with anti-LAG3. As of today, we have presented data in the third line or greater settings from 12 patients using various doses of COM701 with or without nivolumab across studies, and we have shown encouraging preliminary anti-tumor activity with an overall response rate of 8%, including one partial response lasting 44 weeks. Our clinical data from the COM701 nivolumab dose escalation cohort expansion study in a small number of MSS-CRC patients show a modestly higher response rate compared to what has been reported for standard of care. We believe that this initial data, along with the translational package showing the COM701-driven mechanism in MSS-CRC patients, warrant further evaluation of COM701 in a triple combination in a single-arm study. Next, non-small cell lung cancer is an indication we selected as high priority due to clinical landscape and regulatory considerations; as an inflamed tumor type sensitive to PD-1 and possibly TIGIT checkpoint, non-small cell lung cancer may have an increased probability of responding to our triplet combination. We specifically plan to focus on post anti-PD-1 non-small cell lung cancer patients, as we described a high unmet need in the patient population where positive data may allow us to more easily exemplify the uniqueness of our drug in a single-arm triple combination study than in a first-line patient population study where the response rate and duration of response are already high with other checkpoint inhibitors. In addition, a first-line setting presents significant hurdles in patient enrollment due to competitive reasons and therefore may pose a risk in delay to reach data readout milestones. In parallel to this triplet checkpoint study, we also plan to separately evaluate the blockade of PVRIG and TIGIT in combination with standard of care in this patient population. This will allow us to build an additional path to randomized studies and generate insights regarding DNAM axis activity in the presence of chemotherapy. As previously communicated, we plan to share the microsatellite stable colorectal cancer data from the COM701 nivolumab cohort in Q4 of this year. Given our strategic decision to end the cohort expansion studies early, a year and a half prior to projected completion of enrollment and focus our efforts on the prioritized indications, we do not currently plan to present data from the other cohorts. Our focus will be on effective execution of our studies for these prioritized indications, continuing our track record in execution. We plan to expand the protocol of the existing COM701 plus COM902 study and conduct three single-arm studies, each consisting of up to 20 patients, with an aim to enrich for patients who are most likely to respond based on the data we have, what has been reported by others, and discussions with key experts in this indication. The details of the design and the timeline will be shared once finalized in the fourth quarter of this year. We plan to share initial findings and progress of these studies during 2023. Moving on to our core research programs. Compugen scientists are pioneers. We continue to do groundbreaking work focusing on modulating the immune suppressive cells in the tumor microenvironment. We are advancing several early-stage programs, all predicted by our computational discovery capabilities, with one program entering pre-IND enabling studies with first-in-class potential. We are very excited about this program, which is targeting a soluble immune checkpoint upregulated in the tumor microenvironment in response to IFN-γ. We developed a very high affinity antibody, COM503, to block this soluble immune checkpoint pathway, and we believe we are the first to do so. We have demonstrated preclinical in-vitro and in-vivo activity as monotherapy and in combination across various models. We plan to share details on this program in the fourth quarter of this year. And finally, Compugen closed the quarter ended June 30 with $97 million in cash. This strong financial position should allow us to execute on our clinical plans and support our operations through the end of 2024. Before I pass over to Ari, I want to take a moment to thank the Compugen team for their dedication and commitment to the company goals in the second quarter of the year. I also would like to thank Ari, who has agreed to continue to support Compugen while we are in the process of identifying his successor.

Thank you, Anat. Our financial results for the second quarter of 2022 are in line with our forecast and working plans. As of June 30, 2022, we had approximately $97 million in cash, compared with approximately $118 million of cash as of December 31, 2021. Cash balance at the end of 2022 is expected to be in the range of $70 million to $74 million. The company has no debt. As a result of our decision to end our Phase 1 program and focus on two prioritized indications, we expect our ongoing cash expenditures starting in 2023 will be lower by approximately 20% than the current run rate, which is expected to extend the cash runway through the end of 2024. We reported a net loss for the second quarter of 2022 of $9.1 million or $0.11 per basic and diluted share, compared with the net loss of $9.5 million or $0.11 per basic and diluted share in the comparable period of 2021. Research and development expenses for the second quarter of 2022 were $6.8 million, which reflects no change from the comparable period in 2021. Our current level of R&D expenses reflects activities associated with the various ongoing clinical studies as well as expenses associated with our earlier stage programs. Going into the second half of 2022, the reduction in expenses is expected to be limited and will reflect winding down expenses of the current ongoing studies, as well as preparation for the new planned prototype studies. We expect that the full effect of the reduction in expenses will be reflected only in 2023. Regarding G&A, G&A expenses for the second quarter ended June 30, 2022, were $2.6 million compared with approximately $2.7 million for the comparable period in 2021. Now, I will turn the call back to Anat.

In closing, Compugen has done groundbreaking work on the DNAM hypothesis and is well positioned to be a leader in this new area of cancer immunotherapy. We have taken the decisive action to focus our resources on two prioritized indications, taking advantage of having two fully owned clinical assets. Results will guide our future path to registration, and we plan to share progress and initial findings from these studies during 2023. We're making progress on our preclinical pipeline and are very excited about our lead program, which has first-in-class potential and expect to provide more detail by the end of the year. We have a strong balance sheet with a cash balance of $97 million that will support our clinical program and our operations through the end of 2024. I firmly believe we have the right talent to be successful. We have adapted in response to the challenging market conditions, and I believe that with the potential value of our assets and the expansion of our cash runway until the end of 2024, we’re now better positioned to bring value to our shareholders. I’m enthusiastic about what is to come for Compugen and look forward to updating you on our progress throughout the rest of the year. Thank you all for joining us today and taking the time to follow the company.

Thank you. Ladies and gentlemen, we will now start the question-and-answer session. The first question is from Stephen Willey of Stifel. Please go ahead.

Hi. This is Bonnie Quach on for Steve Willey at Stifel. Was the non-small cell lung cancer indication previously earmarked as a tumor type of interest for any of these expansion cohort combo trials, both double and a triplet? And if not, does this represent a change in the PVRL2 expression guided selection of tumor types for the DNAM-1 pathway inhibition? I know the CRC indication was selected not because of PVRL2 expression, but because of signals you observed in the Phase 1 dose expansion results.

Non-small cell lung cancer has always been recognized as an indication where the PVRIG pathway should be active. We conducted a small monotherapy study for this indication and have shared the data, which I will let Henry also discuss. Non-small cell lung cancer remains unchanged in our approach. We decided to advance with this indication because it shows inflammation where we believed from the outset that PVRIG should be effective, and we have encouraging data to support this. There is already publicly available information that justifies our focus on it. This inflamed indication is quite different from the cohort studies we were pursuing, which were aimed at hard-to-treat patient populations who are resistant to checkpoint therapies. This represents an addition rather than a shift from our original predictions. Eran, would you like to add anything?

Yeah. Actually, non-small cell was definitely identified by us as one of the indications initially that was published in our papers that non-small cell lung, ovarian, and others are the indications with the highest expression of the pathway. I will let Henry know this probably be the results that we already showed on non-small cell.

Thank you, Eran and Anat. During this escalation, we also presented this data at ASCO over the past few years. We found that five out of the seven subjects enrolled in the study experienced stable disease during this escalation. These subjects demonstrated durable stable disease, with at least two of them maintaining stability for six months or longer. Additionally, we observed that these subjects appeared to perform quite well overall. Upon reviewing the therapies they underwent, we noted that all had received immune checkpoint therapy. This led us to confirm a potential signal in post-IO non-small cell lung cancer, which is supported by the preclinical data that Eran just mentioned.

Okay, great. Thanks. Since you've indicated that you'll still be evaluating a triplet combination, does it mean that you're interested in securing another clinical collaboration to gain access to an anti-PD-1 antibody? Please correct me if I'm wrong, but I believe the MOI previously had the right of first refusal on any COM701 partnership. So does that remain with the conclusion of the clinical collaboration?

Yes, I mean, from the perspective of having access to PD-1. Not necessarily for these studies; we don't have to have a partner. We're not ruling out entering into additional collaborations in the future on this asset, obviously. But no, these are small studies, very focused, designed well in order to maximize the effect and ensure that we have the highest probability of success. When we stated in the prepared remarks that we can extend the cash runway, everything is built into it, and we're taking it into consideration. So no, not necessarily, but as I said, we're not ruling it out. In terms of the right of first negotiation for Bristol or any other rights, know that the collaboration is terminated, and we're independent. We will keep the flexibility that we have to do the studies at the right pace and with a sense of urgency for a small biotech company.

Okay, great. Thank you for taking my questions.

The next question is from Mark Breidenbach of Oppenheimer. Please go ahead.

Hey. Thanks for taking the questions and congrats on coming to this strategic decision. I guess it would be helpful maybe for Anat or Eran to highlight any key mechanistic differences between COM902 and the Bristol Myers Squibb TIGIT antibody, both in terms of effects on immune cells and maybe just differentiating factors between how they interact with TIGIT. Why should we expect one to behave differently from the other in the clinic? And then another question I had, I think I’ve heard Anat mention there was an 8% overall response rate in MSS-CRC patients from your prior trials. I just wanted to make sure that's not inclusive of the expansion cohort that you've been running, and that we're expecting to see some data from in the fourth quarter. Thank you.

Correct. I'll relate first to your second question. Correct, this is not included.

Yes. And for COM902 versus BMS TIGIT. So first of all, BMS TIGIT is the IgG1 mutated, and COM902 is IgG4. Now relating more generally to COM902 without the comparison specific to BMS TIGIT for obvious reasons, but when you compare COM902 to most of the leading assets for other competitors. What we have seen and presented is that COM902 has better affinity, better blocking, and as good or better functional activity in enhancing T-cell activation. In general, we have a high-affinity antibody that is capable of saturating the target in low concentrations, and we think we have a robust in-class potential.

Okay. Thanks so much.

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

Hello. This is Asthika at Truist. What will happen to the endometrial and ovarian cohorts now that CRC and non-small cell are prioritized? Previously, you mentioned that enrollment across all cohorts was projected at about 20 patients each by the end of 2023. Does that still apply to endometrial and ovarian? Additionally, how much data should we anticipate for CRC in the fourth quarter? Will it be around 20 patients as well? And what will the follow-up period be for those patients? Thank you.

Yes, as we mentioned today, we are going to close the cohort in the expansion studies across all the studies. This decision comes a year and a half before the study's conclusion. You are correct that completion of enrollment was initially planned for the end of 2023. I want to emphasize that our decisions are well-informed and bold. We believe that with our insights and current market conditions, as well as our ability to concentrate on the triplet and two indications, this is the best path forward. We will close the studies while ensuring patient safety for those currently in the study or those who are about to be enrolled. We are working closely with Bristol Myers Squibb, and I want to express our gratitude for our fruitful collaboration. We have supported each other and gained valuable knowledge. Now is the time for us to advance into focused studies that are well-informed and for us to execute quickly as a small biotech company. Regarding the Q4 data, we have reiterated our guidance. It pertains to the CRC data from the COM701 volume study in an expansion cohort of 20 patients. Any insights we gain from CRC will be shared and will help inform the design of the studies we plan to conduct, so we are on track.

Great. Just a follow-up. So for the 701 monotherapy, will the ovarian, breast, and endometrial cohorts still be enrolling at some point, or are those going to be closed as well?

So the monotherapy, the small monotherapy study that we did with the five indications has already completed enrollment a long time ago and we shared all the data from this study. So, no, the studies that are currently ongoing and will be closed are the triplet and doublet.

Okay, so we can expect further development of ovarian, breast, and endometrial, just to clarify for the 701?

Not at this point in time. Currently, we follow the insights and we’ll focus on CRC. We want to add an inflamed indication, which makes sense for us to add. We're flexible to move forward on these two indications, and this is what we will do. It doesn’t mean that in the future, we won’t open additional indications. But for right now, this is the right decision for us.

Perfect. Thank you so much. I appreciate it.

The next question is from Tony Butler of Roth Capital. Please go ahead.

Thank you very much. I want to clarify the situation regarding the Bristol collaboration and its conclusion. Compugen will still have access to nivolumab, meaning there will be no need to pay Bristol for nivolumab in the upcoming studies related to non-small cell lung cancer and CRC. That’s my first question; I just wanted to confirm that. For my second question, Eran, you mentioned this before, but I want to verify again: non-small cell lung cancer is a PVRL2 high expressing tumor. What about CRC, considering it is a non-inflamed tumor? Generally speaking, does it also have very high levels of PVRL2 in third and subsequent lines of therapy, similar to non-small cell lung cancer? Thank you very much.

So I will start with the nivo question. First, we will share the design. It is not given that it will be nivo that we will pick. There are different considerations, and this is not we were concluding the collaboration with Bristol Myers Squibb. So we have a good relationship, definitely, but we have no additional arrangements that are following this determination, and we will buy the PD-1 checkpoint that we will pick to use that we will share, obviously. As I said, the cost of buying the PD-1 inhibitor is already calculated into the resources that we'll need to allocate for these studies, and it is already calculated into what we're saying there that we're extending the cash until the end of 2024. All of it is already accounted for.

For your question about PVRL2. So if I understood the question correctly, PVRL2 is not expressed in relation to the inflammatory status of a tumor environment, meaning PVRL2 can be expressed high or low across tumor types, regardless of PD-L1 expression. So you can find PVRL2 high also in tumors which have less PD-L1. So we have relatively high PVRL2 in CRC, and we also saw the clinical signals, and that's why we're following this indication. We also see high expression in PD-L1-higher indications like non-small cell lung cancer. So these two indications have high expression of PVRL2 and in general the PVRIG pathway regardless of the PD-L1 status of the tumor.

I understand that. Just one follow-up. It was the notion of actually both being, let's just call it, you said moderately high, I think CRC. And so the question really is, is it as high as non-small cell lung cancer or less than, just to get a relative?

Relatively, I would say that CRC was not pre-identified initially as one of the highest indications where non-small cell lung cancer was, but it definitely has high expression of the pathway. We also saw clinical signals, and that's why we're following this indication, of course. It also gives us high expression in PD-L1-higher indications like non-small cell lung cancer.

Thank you very much. Appreciate it.

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

Hi, guys. Thank you for the questions. First, I want to clarify the information that you used to make the strategic decision. Specifically, did you review any of the ongoing cohort expansion, the CRC, or any of the others, and how much did that review of ongoing data inform this decision?

Yeah. A few things. First, we're trying to share some insights from the expansion cohorts that we have shared today. We stated that we see initial signals of anti-tumor activity. We also have some insights regarding the contribution of components and the translational work that was already done. Obviously, the studies are ongoing, and we don't have everything in front of us, but part of the translational work is suggesting that what we see is actually COM701 mediated, and that's related to the COM701 mechanism of action. This was one driver that made us decide to focus and not to continue a broad assessment of three studies, many patients in many indications. We wanted to be faster on this and increase the probability of success. I'll also say that at the end of the day, it is not only a cash-wise decision, not at all. We were also thinking about how we translate what we have in hand into a more cash-sensitive approach. So we'll be able, in these market conditions, to extend the cash runway but still focus on the assets that we have and give them the highest probability of success. I also want to mention that we did not under these studies; we did not start TIGIT. With the path forward for our TIGIT studies, we believe it will make sense for us to use our own TIGIT, where we really believe in it. We think that it's first-in-class. We have data to support that, and we believe that we can add our own TIGIT and move forward. So that covers the totality of the reasons.

Perfect. Two more follow-up questions. If we were not in this market situation and you had significantly more cash resources, how might the strategy now be different if you were refocusing?

It's a very good question because I did start the answer by telling you that it is not a cash-only decision. It is not. It adds complexity, but it is not. I guess that if we would try to trim the studies less, we could focus maybe on more indications in parallel, but with that in mind, I'll tell you that we feel very strongly that what we're doing now is not compromising on our ability to exemplify the value of COM701 and also COM902. We feel comfortable that this is the right decision. Still, if cash were totally not an issue, then probably we would be looking at things a little differently.

Perfect. One last question around BMS. Was this decision to move away from the collaboration instigated by you, Compugen, or did this come at all from BMS?

It is by Compugen. Obviously, it was done in a very good relationship with Bristol Myers Squibb. We appreciate them a lot, but it is our decision, and I want to elaborate on it because it is a very important question. It is not that we made the decision to stop the collaboration with Bristol Myers Squibb and then no, we made the decision to focus the studies. We felt that what we have is very reasonable for us to not wait until the end of the studies to close everything. We thought that this was the right time to not move ahead, to focus, to be nimble, to be fast, to give it the highest probability of success, and we see it now. The highest probability of success will result from closing the studies and ending the collaboration.

That's very helpful. Thank you so much.

The next question is from Reni Benjamin of JMP Securities. Please go ahead.

Hey, guys. Thanks for taking the questions. Just going back to the whole BMS termination, I understand what you're saying, Anat, but I guess I'm kind of curious a little bit more in terms of where other options explored. For example, could you have restructured the current collaborations so you could continue to get the volume up? I just want to know if there were any other options available or if terminating was the only way to go?

It was a well-thought-out and informed process. It was not a decision that was taken lightly. We understand the implications of all of these moves, but we thought that they are advantageous for Compugen, and getting nivo for free for the studies that we want to do is a consideration. But it is not the main consideration, obviously, because these are small studies and we can afford it. If we had to conduct much larger studies, maybe that would have been a different situation. But at this point in time, we can do it. We have been doing all the studies up until now, right? It has been our execution. So yes, we were internally exploring different options and had discussions with BMS, but as I said, it was our decision, and we feel very comfortable saying that it's the right decision at this time.

I joined the call a bit late, so you might have already addressed this, but regarding the COM701 and nivolumab data, could you elaborate on the clinical data showing a slightly higher response rate? When I think of a slightly higher response rate, it seems to me that a confirmatory study would need to be quite large to detect that difference. Were there any additional clinical insights that are guiding you towards this specific indication in combination, or are we waiting for the complete dataset before making a decision on the next steps?

From our perspective internally, we're at the stage of the design, and obviously we will share the design and the path forward in Q4 for the call. I will say that it’s a different question, and I'll address it. At the end of the day, we have 20 patients, and MSS-CRC is an ultra-hard to treat indication. The lines that we're treating, even after Lonsurf and regorafenib, are ultra-hard to treat. So when you're looking at the patient population where the response rate for Lonsurf and regorafenib is 1% and you're working with small numbers, I think it is very reasonable to define it as more-depth clinical work. I will state that it is not only the response rate that we're looking at; we were referring to the response rate in the press release and in the prepared remarks. The fact that we believe that what we see is the COM701 biology; it is driven by the COM701 mechanism of action, gives us more confidence. Going forward, we stated that we're going to collect the triplet in this indication, so this will give us the maximum blockade of the DNAM axis. We will hope to maximize the effect and hope to increase the confidence that we can inform our path forward. But in Q4, we'll share a path forward with the new study, which can give some insights into how we're going to relate to it going forward, but it will not be a plan to the next hopefully randomized studies that we will be able to.

Got it. Okay. Thanks for that clarification. And I guess just finally for us, I would love to get your thoughts around Roche's disclosure at ASCO, that the majority of their statistical power was allocated in their trials towards OS versus PFS. And kind of like a rejuvenation, I think, of hope for the TIGIT assets in general. Can you maybe comment on how that disclosure may be impacting your plans or thinking going forward?

I think on the Roche data, I think there’s so much being said. I think we all need to wait for the overall survival. We think it's a big enough program. At this point in time, the TIGIT space is quite significant. We investigated this pathway alone, as well as part of the DNAM axis with PVRIG, and we have so much knowledge at Compugen on this pathway and the science behind it; we have been speaking about it for years. We are optimistic with respect to TIGIT. We don’t know what would be the impact: Would it be very dominant or less dominant? Is the exact patient population, etc.? We believe that it’s a pathway that is valid to follow, hence our decision also to focus on our own TIGIT, COM902, and do the studies with our own COM902. That’s how it informed our decision; it was not the main reason why we decided to change, but it was another consideration that we were looking at.

Got it. Thanks for taking the questions.

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 your concluding statement?

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

Thank you. This concludes the Compugen Ltd. second quarter 2022 financial results conference call. Thank you for your participation. You may go ahead and disconnect.