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spk05: 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 investors section of CompuGen's website, www.cgen.com. As a reminder, today's call is being recorded. I would now like to introduce Yvonne Naughton, Head of Investor Relations, and Corporate Communications. Yvonne, please go ahead.
spk08: Thank you, Yoni, and thank you all for joining us on the call today. Joining me to present prepared remarks are Dr. Anak Cohen-Dyag, President and Chief Executive Officer, and Ari Krashen, Chief Financial and Operating Officer. For the Q&A session, we will also be joined by Dr. Henry Adewoye, Chief Medical Officer, and Dr. Eran Ofer, Senior Vice President, Research and Drug Discovery. 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, 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 filing for more details on these risks, including the company's most recent annual report on Form 20F, 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.
spk01: 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 insights to focus on two prioritized indications and wind down the existing cohort expansion studies in our current phase one program. Our focus development plan results in the strategic decision to wind down these studies, resulting in the conclusion of our collaboration with Bristol-Mass Squibb. I would like to thank them for our productive interactions and for supplying nivolumab and their anti-tigit antibody for our Phase I program, enabling us to initiate the triple and dual combination studies to evaluate our denim 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, site 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 I studies is the right thing to do at this time. We at Compugen 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 a future path to registration. Second, under these market conditions, It reduces the risk posed by a further broad assessment of three large parallel studies in hard-to-treat immune checkpoint inhibitor insensitive indications and with patients who 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 switch to and develop our differentiated anti-tigit antibody COM902. And finally, it gives us flexibility and provides us with 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 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 the rationale behind our strategic decision to conclude our current phase one program early, our choice of prioritized indications and path forward, I will also briefly touch on advancement 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 anti-tigit 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 science. CompuGen is the only company studying the triple blockade of the Dynamaxis targeting PVRIG, TIGIT, and PD-1 in the clinic. We're leading the way and others are following. We recognize targeting TIGIT is a competitive space with the most advanced programs already being evaluated by pharma in phase three studies. This is testament to the promise of modulating this pathway to enhance anti-tumor immune responses. Importantly, we believe that not all TGs are the same. We were the first company to present clinical data with an IgG4 anti-TG antibody with low FC effect or function, and we have good reason to believe this is the right design to pursue. And in contrast to others, we have shown clinically that COM902 avoids depletion of CD8 plus T cells, the cells important for antitumor activity. We believe the IDG4 backbone may come with additional efficacy and 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 biology 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 in 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. moving to our strategic decision to advance two prioritized indications and end our Phase I cohort expansion studies. Our Phase I cohort expansion program was designed to allow us to systematically evaluate our hypothesis that simultaneously blocking three pathways, PDR-IG, 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 an intention to learn as much as possible on 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're able to detect immune activation suggesting a COM701-mediated mechanism of action. We believe the initial signals of antitumor activity that we're seeing with COM701 coupled with changes occurring in the tumor microenvironment in some of the hard-to-treat checkpoint nonresponsive 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 a future path to registration. One in a less inflamed tumor, microsatellite-stable colorectal cancer, with a low bar to beat 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 cancer in anti-PD-1 treated patients. This tumor type is more immunologically responsive and therefore may present a more permissive environment for denim axis activity, although the patient population is challenging to treat. Going back to microsatellite-stable colorectal cancer, there is no approved therapy specifically for this patient, 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 Lonserve, which show overall response rate of 1%, median progression-free survival of two months, and median overall survival of six to seven months. Also note, Pembrolizumab monotherapy has shown 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 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 antitumor activity with an overall response rate of 8%, including one partial response of 44 weeks. Our clinical data from the COM-701 Evolumab dose escalation and 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 COM-701-driven mechanisms in MSS-CRC patients, warrants further evaluation of COM71 triple combinations in the single-arm study. Next, non-small cell and cancer, 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 TG checkpoints, non-small cell and cancer may have an increased probability of responding to our triplet combination. We specifically plan to focus on post-NTPD1 non-small cell and cancer patients as it describes a high unmet need and the patient population where positive data may allow us to more easily exemplify the uniqueness of our drugs in a single-arm triple combination study as opposed to 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 present a risk in delay to reach to data readout milestones. In parallel to this triplet checkpoint study, We also plan to separately evaluate the blockade of PD-RIG 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 the Dynamaxis activity in the presence of chemotherapy. As previously communicated, we plan to share the microsatellite-stable colorectal cancer data from the COM701 EVOLUMAB cohort in Q4 of this year. Given our strategic decision to end the cohort expansion studies early, a year and a half prior to projection 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 the three single-arm studies. Each will consist 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 these indications. The details of the design and the timelines 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, competent 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 interferon gamma. We developed a very high affinity antibody, COM503, to block this targeted soluble immune checkpoint pathway, and we believe we're 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.
spk06: 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 31st, 2021. Cash balance at the end of 2022 is expected to be in the range of $72 to $74 million. The company has no debt. As a result of our decision to end our phase one 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 11 cents per basic and diluted share, compared with a net loss of $9.5 million, or 11 cents 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 reflect the 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 prioritized 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, with $2.6 million, compared with approximately $2.7 million for the comparable period in 2021. Now, I will turn the call back to Anat.
spk01: In closing, CompGen 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 extension of our cash runways with the end of 2024, we're now better positioned to bring value to our shareholders. I'm enthusiastic for 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.
spk05: Thank you. Ladies and gentlemen, at this time we will begin the question and answer session. If you have a question, please press star 1. If you wish to decline from the polling process, please press star 2. If you are using speaker equipment, kindly lift a handset before pressing the numbers. Please stand by while we poll for your questions. The first question is from Steven Wiley of Stifel. Please go ahead.
spk09: Hi, this is Bonnie Quach on for Steve Wiley 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 the doublet and the triplet? And if not, does this represent a change in the PVRL2 expression guided selection of tumor types for the DNAM1 pathway inhibition? I know the CRC indication was selected not because of PVRL2 expression, but because of signals you observed in the phase one dose expansion results.
spk01: So non-small cell and cancer was always an indication that we were stating that it's an indication where the PVRIG pathway should be active. And I later on shared some of the data that was leading us to this. Also, we were testing the non-small cell and cancer indication in the monotherapy, small monotherapy study that we did, And we shared the data, and I will let Henry also relate to it as well. So, no, non-small cell cancer is totally not a change. And the reason that we decided to move forward with this indication is really it's an indication that is an inflamed indication where we saw that PVRIG from the beginning should work and that we have some data that is encouraging. There is already in the public domain that... um that makes sense for us to follow and the fact that it is an inflamed indication is very different from the cohort studies that we that we were pursuing as part of the extension cohort studies which were focused only on how to treat patient populations and checkpoints insensitive so this is an addition but it's totally not a situation where it was not predicted to begin with Iran do you want to add anything about
spk07: Yeah, actually, non-small cell was definitely identified by us as one of the top indications initially from the beginning, also published in our papers, that non-small cell along ovarian and others is one of the indication which highest expression of the pathway. And I will let Henry now describe a bit the results that we already showed for non-small cell.
spk10: Yes, thank you so much, Eran and Anat. So during this escalation, and we've reported this data also at ASCO in the last couple of years, We observed that we had five subjects with stable disease of the seven subjects that were enrolled onto the study during this escalation. And these subjects had durable, stable disease with at least two of those subjects with durable, stable disease beyond at least six months or more. The other thing that we did observe was that, and we reported on this, was that these subjects appear to have done very well. And we've gone back to look at the therapies that they received, and all have received immune checkpoints. So, those are the things that led us to confirm that there seems to be a signal also in post-IO non-small cell lung cancer supported by the preclinical data that Eran has just mentioned.
spk09: Okay, great. Thanks. And since you've indicated that you'll still be evaluating a triplet combination, Does this mean that you're interested in securing another clinical collaboration to gain access to an anti-PD-1 antibody? And please correct me if I'm wrong, but I believe the MOI previously had the right to first refusal on any COM-701 partnership. So does that remain with the conclusion of the clinical collaboration?
spk01: So, yes, I mean, from the perspective of having an 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 in order to make sure that we have the highest probability of success. And when we were stating in the prepared remarks that we can extend the cash runway, et cetera, everything is built into it and we're taking it into consideration. So no, not necessarily, but as I said, we're not ruling 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 and we will keep the flexibility that we have in order to do the studies in the right pace and with a sense of urgency for a small biotech company.
spk09: Okay, great. Thank you for taking my questions.
spk05: The next question is from Mark Breidenbach of Oppenheimer. Please go ahead.
spk02: Hey, thanks for taking the questions and congrats on coming to this strategic decision. I guess it would be helpful maybe for Anat or Iran maybe 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 TGA, why we should expect one to behave different from the other in the clinic. And then another question I had, I think I heard Anat mention there was an 8% overall response rate in MSF-CRC patients from your prior trials. I just wanted to make sure that that's not inclusive of the expansion cohort that you've been running that we're expecting to see some data from in fourth quarter. Thank you.
spk01: Correct. I'll relate first to your second question. Correct. This is not included.
spk07: Yeah, and for CommonLN02 versus BMS-TGIT. So, first of all, the fact is that BMS-TGIT is IgG1 mutated and CommonLN02 is IgG4. Now, relating more generally to CommonLN02 without the comparison of specific to BMS-TGIT for obvious reasons, But when you compared COM902 to most of the leading assets for other competitors, what we have seen and presented that COM902 has better affinity, better blocking, as good or better functional activity in enhancing T-cell activation. So in general, we have a high affinity antibody to be able to saturate. We also presented that saturated target in low concentration, and we think we have a best-in-class potential.
spk02: Okay, thanks so much.
spk05: The next question is from Astika Gunwardhan of Truist Securities. Please go ahead.
spk03: Hello, this is Anaj Kaner on for Astika at Truist. What's going to happen to the endometrial and ovarian cohorts now that CRC and non-small cell are priority? I know previously you had said that enrollment across all cohorts, about 20 patients each, was projected for end of year 2023. So does that still hold for endometrial and ovarian? And then secondly, how many patients' worth of data should we expect in 4Q for CRC? Is that about 20 as well? And how much follow-up for those patients? Thank you.
spk01: So, yes, as we stated today, we're going to close the cohorts in the expansion studies, in all the studies, It's a decision that we are taking a year and a half before the end of the study. You are correct. The completion of enrollment was scheduled for end of 2023. I think that, you know, I'll say to the management that the decisions that we're taking are really well-informed but bold and decisive, and we do think that with the insights that we have, And with the market conditions and the fact that we can focus on the triplets and T-indications, that's the right way to go. So this is what we do. We will close the studies. Obviously, we'll take care not to harm any patients, the patients that are on the study or are about to be enrolled, are going to be enrolled. We are working very closely with Bristol-Mers-Quebec. In general, I'll have to say, I was saying it in the prepared remarks, But I still say that we thank them a lot. It was a fruitful collaboration, and they supported us, and we learned from each other. But now is the time for us to move ahead and move into focused studies, well-informed, and to execute, as I said, as a small biotech company quickly. So this is it. And for the Q4 data, Yes, we repeated the guidance that we gave. It's the CRC data from the COM701 Nivolumab study, and it's an expansion cohort of 20 patients. Whatever insights that we'll have on CRC, we will share. Obviously, this will inform the design of the study that we're aiming to do, so we're on it.
spk03: Great. And then just to follow up, so For the 701 monotherapy, the ovarian, breast, and endometrial cohorts, are those still going to be enrolling at some point, or are those going to be closed as well?
spk01: So the monotherapy, the small monotherapy study that we did with the five indications already completed enrollment long ago, and we shared all the data from this study. So, no, the studies that are currently ongoing and will be will be closed are the triplets and the two doublets.
spk03: Okay, so we can expect further development of ovarian breast and endometrial, just to clarify, for the 701 level.
spk01: Not at this point in time. 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 and we're flexible to move forward on these two indications, and this is what we will do. And it doesn't mean that in the future we're not going to open additional studies in additional indication, but for right now, this is the right decision for us.
spk03: Perfect. Thank you so much. I appreciate it.
spk05: The next question is from Tony Butler of Roth Capital. Please go ahead.
spk04: Thanks very much. Annette, I want to clarify ending the Bristol collaboration, Compugen will still receive or be able to obtain nivolumab. In other words, you will not need to actually pay Bristol for nivolumab in the subsequent studies in non-small cell lung cancer and CRC. That's question one. I just want to clarify. And then in question two, Iran may have said this, or partially said this, but I want to clarify again. Non-small cell lung cancer was a PVRL2 high-expressing tumor. What about CRC, it being a non-inflamed tumor? Does it, generally speaking, post, let's just call it third and subsequent lines of therapy, also have very high levels of PVRL2 similar to that of non-small cell lung cancer. Thanks very much.
spk01: So I will start with an EVO question. So first, we will share the design. It is not given that it will be an EVO that we will pick. There are different considerations, and this is not. We were concluding the collaboration with Bristol Mass Quibs. So we have good relationship, definitely, but we have no additional arrangements that are following this termination. And we will buy the PD-1 checkpoint that we will pick to use, that we will share, obviously. And as I said, the cost to buy the PD-1 inhibitor is already calculated into the and the resources that we will need to allocate for these studies and it is already calculated in what we're saying that we were extending the cash until the end of 2024 all of it is already calculated in it thank you and then for a question about people too so if i got the question right fever l2 is not expressed in relation to the inflammatory status of the tumor environment meaning
spk07: you have PvRL2 high or low expression 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 on CRC, and we also saw the clinical signals, and that's why we're following this indication, of course. And we have also PvRL2 high expression also in PD-L1 higher indication like non-small cell lung cancer. So these two indications have high expression of PvRL2, and in general, the PvRLG pathway And this is regardless of the PD-L1 status of the tumors.
spk04: 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, of 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...
spk07: Relatively, I would say that CRC was not pre-identified initially as one of the highest, highest indication, while non-sponsored cancer was, but it definitely has high expression of the pathway, and when we also saw the clinical signals, it was, again, one of the indications that was not initially the top priority, but in combination with the clinical signals, it was an easy choice to move forward with this one.
spk04: Thank you very much. Appreciate it.
spk05: The next question is from Dana Graybosh of SVB. Please go ahead.
spk12: Hi, guys. Thank you for the questions. First, I want to clarify the information that you used to make the strategic decision. So specifically, did you review any of the ongoing cohort expansions, the CRC or any of the others? And how much did that review of the ongoing data inform this decision?
spk01: Yes, so a few things. So first, we're trying to share today some insights from the expansion cohorts that we have, and we stated that we see initial signals of anti-tumor activity, and we also have some insights with respect to the contribution of components, and also And the part of 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 COM 701 mediated and that relates to the COM 701 mechanism of action. So this is one driver that made us to make this decision to focus and to, not to continue a very broad assessment of three studies, many patients in many indications. So we wanted to be faster on this and increase the probability of success. I'll also say that obviously at the end of the day, it is not only a cash wise decision, not at all, but also we were thinking how we translate what we have in hand into some more cash-sensitive approach. So we're able, in these market conditions, to extend the cash runway, but still focus on the assets that we have and give them the high probability of success. Also, I want to mention that, obviously, we did not, under these studies, we did not test our fidgets. And with the path forward for our TIGIT, we saw that if we're making this change, it will just be very reasonable for us to use our own TIGIT where we really believe in it. We think that it is first in class. We have data to support our belief in it. So we saw that that could be an edge for us just to add our own TIGIT and move forward. So Dana, that's more or less the totality of the reasons. Perfect.
spk12: So two more follow-up questions. If we were not in this market situation and you had significant more cash resources, how might the strategy now be different if you were refocusing?
spk01: Yeah, it's a very good question, you know, because I did start the answer by telling you that it is not cash-only decision. It is not. It adds, but it is not. I guess that if we would try to be, we would trim less the studies, I guess. We would focus maybe on more indications in parallel. But with that in mind, I'll tell you that we feel very strongly that that what we're doing now is not compromising on our ability to exemplify the value of COM701 and now, by the way, also COM902, and that we feel comfortable that this is the right decision. Still, you know, if cash is totally not an issue, then probably we would trim a little bit less.
spk12: Perfect. And then one last question around BMS. Was this decision and moving away from the collaboration instigated by UCOMPIGEN, or did this come at all from BMS?
spk01: It is by Compugen. Obviously, it was done in great, in very good relationship with Bristol-Myers Squibb. We appreciate them a lot, but it is our decision, and I want to, it's a very important question. I want to elaborate on it. It is not that we made the decision to stop the collaboration with Bristol-Myers Squibb, and then we, no. We made the decision to focus the studies we thought that with what we have, it is very reasonable for us not to wait an additional year and a half until we close all the studies and finish the collaboration and decision-making for BMS. We thought that this is the right time not to move ahead with this, to focus, to be nimble, to be fast, to give it the highest probability of success. As we see it now, the highest probability of success And due to this, due to the fact that we're closing the studies, it is obviously the end of the collaboration. Yes, it was ours. That's very helpful.
spk12: Thank you so much.
spk05: The next question is from Wren Benjamin of JMP Securities. Please go ahead.
spk11: Hey guys, thanks for taking the questions. Just going back to the whole BMS termination, I understand what you're saying and not, but I guess I'm kind of curious a little bit more in terms of where other options explored. So for example, could you have restructured the current collaboration so that you could continue to get the volume map? I just want to know if there were any other options that were available or, you know, terminating was the only way to go.
spk01: So, obviously, Rene, it was a well-thought and well-informed process. It was not a decision that was taken lightly. We understand the implications, all of them, but we thought that there are advantages for Compugen and getting NEVO 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. And at the end of the day, you know, I mentioned it as well, we have our own COM902. We believe in our assets and we would like to test it. And it gave us an opportunity. Probably if we would go to much larger studies, maybe that was a different situation. But, you know, at this point in time, we're equipped to do it. We can do it. We were doing all the studies up until now, right? It's our execution. And so, yes, we were internally, we were exploring different options. We had discussions with BMS. But as I said, it was our decision, and we feel very comfortable to say that at this point in time, this is the right decision. It didn't make sense for us to move forward with this, to continue to pursue this study.
spk11: Got it. And I jumped on the call a little late, so you may have answered this, but when you talked about the COM701, the Volumab data, clinical data, showing a modestly higher response rate. Can you maybe provide some color around that? When I think modestly higher, I automatically think that the confirmatory study is gonna have to be quite large in order to detect that modestly higher response rate. Were there any other clinical clues, if you will, that are pushing you towards this particular indication and combination? or are we kind of waiting for the full data set to come out before you make a decision regarding the path forward?
spk01: No. So from our perspective internally, we're at the stage of the design, and obviously we'll share the design and path forward in the Q4 call. I will say that it's a fair question, and I'll address it. Look, at the end of the day, we have 20 patients, And MSS-CRC is an ultra-high to treat. And the lines that we were treating, right, even before, even after Lonesurf and Regorafenib, it is ultra-high to treat, ultra-high to treat. So when you're looking at the patient population where the response rate for Lonesurf and Regorafenib is 1%, and you're working with small numbers, I think that it is very reasonable to define it as modest. I will say that it's not only the response rate that we were looking at, although we were referring to the response rate in the press release and in the prepared remarks, but the fact that we believe that what we see is the COM-701 biology. It is driven by the COM-701 biology, by its mechanism of action, gives us more confidence. Going forward, we stated that we're going to test the triplet in this indication. So this will give us the maximum blockade of the Dynamaxis. We hope to maximize the effect, and we hope to increase the confidence so it can inform our path forward. But in Q4, we'll share a path forward with a new study, which can give some insights maybe to how we're going to relate to it going forward, but it will not be a plan to the, you know, to the next hopefully randomized studies that we will be able to do.
spk11: Got it. Okay. Yeah, thanks for that clarification. And I guess just finally for us, you know, Would love to kind of get your thoughts around, you know, Roche's disclosure at ASCO that the majority of their statistical power was allocated in their trials towards OS versus PFS, you know, and kind of like a rejuvenation, I think, of, you know, the hope for the TIGIT assets in general. You know, can you maybe comment on how that disclosure may be impacting your plans or thinking going forward?
spk01: So, I think, you know, on the Roche data, I think that there is so much is being said there. I think that all of us will need to wait for the overall survival. I, you know, we think it's a beaten up program at this point in time. The TGIT, in general, the TGIT space, we think too much. I'll tell you, look, we investigated this pathway alone and as part of the Dynamaxis and with PVRIG so much. We have so much knowledge at Compugen on this pathway and the science behind it. And you know that we're speaking about it for years. So, you know, we're optimistic with respect to TG. We don't know what would be the impact. Would it be very dominant or less dominant? Is it the exact patient population, etc.? ? but we believe that it's a pathway that is valid to follow, hence our decision also to focus on our own TGs, on COM902, and do the studies with our own COM902. So this is how it has informed our decisions. It was not the main reason why we decided to change, but it is another consideration that we were looking at.
spk11: Got it. Thanks for taking the questions.
spk05: This concludes our Q&A session. I will now turn the call back to CompuGen's president and CEO. Dr. Cohen-Dayak, would you like to make your concluding statement?
spk01: Yes. Thank you, operator. Thank you all for joining us today and your continued support. Stay safe and healthy.
spk05: 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.
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