Ladies and gentlemen, thank you for joining us today. Welcome to Compugen's Third Quarter 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. Today's call is being recorded, and will be available on the Investor Relations section of our website. Joining me to present our prepared remarks are Anat Cohen-Dayag, President and CEO, Henry Adewoye, Chief Medical Officer, and Ari Krashin, Chief Financial and Operating Officer. For the Q&A session, we will also be joined by Eran Ophir, Vice President Research & Drug Discovery. Leaving slide 2. 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, our business outlook, our development efforts and their outcomes, our 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 cause you that such statements reflect only the Company's current beliefs, expectations, and assumptions, but actual results, performance, or achievements of the Company may differ materially. These statements are subject to known and unknown risks and uncertainties, and we refer you to the SEC filings for more details on these risks, including the company's most recent annual report on forum 20th filed on February 25th, 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.

Slide 3 please. [Indiscernible]. Thank you, Yvonne. Good morning and good afternoon, everyone. And welcome to our Third Quarter 2021 update. Today is an exciting day from Compugen with the announcement yesterday of the expansion of our strategic collaboration with BMS along with $20 million equity investment. And today, with the release of our 3 presentation at [Indiscernible], providing clinical, translational and preclinical data that demonstrate strong execution across our differentiated clinical, and scientific strategy and defer the support to our path forward. Indeed, to our knowledge, this is the first data presentation ever of a treatment blockade of PVRIG, TIGIT and PD-1 and the first-time data on anti-tumor activity of an Fc reduced effector function antithetic antibody is presented in a scientific conference. These dose escalation studies cleared our path to initiate multiple expansion cohort studies, that are designed to broadly evaluate related to [Indiscernible] of the DNAM axis in cancer immunotherapy, and advance [Indiscernible] operating development of our 2 leading programs COM701 and COM902. Henry will review the data from our dose escalation studies in the call. But before that, I'd like to share a high-level overview of the 4 key pillars of our long-term strategy, and an overview of our clinical strategy. Moving to Slide 4. Our first pillar is to advance the field of immuno -oncology research with ultimate goal of developing new therapies. We have an impressive track record of driving the discovery of new targets and pathways in the immuno -oncology space, with cutting edge time published in peer-reviewed papers and development of clinical stage pipeline derived from this time. Our clinically validated computational target discovery platform has generated a pipeline of exciting new candidates that are being evaluated in phase 1 clinical trials by us and our partners, including our potentially first-in-class anti-PVRIG…

Thank you, Anat. So, we'll move to Slide 7, please. I am pleased to provide you with an overview of the preliminary results from our ongoing Phase 1/2 study evaluating the combination of COM701, our potentially first-in-class anti-PVRIG antibody with nivolumab and BMS ' anti-TIGIT antibody BMS-986207 released today at SITC. The study enrolled 13 DLT evaluable patients with a variety of advanced solid tumors. That is all comers who had exhausted all available standard treatments and were heavily pre -treated with a median of 10 prior therapies and a maximum of 19. The study evaluated escalating doses of COM701 in combination with fixed doses of nivolumab and BMS's anti-TIGIT antibody. The primary objective of this study is to evaluate the safety and tolerability of the combination. The study reported, no dose limiting toxicities and the combination had a favorable safety profile and was well-tolerated. Reaching this important milestone, shares the path for a comprehensive evaluation of Compugen's DNAM axis hypotheses of triple blockade of PVRIG, TIGIT and PD-1 pathways in select biomarker informed indications. Additionally, COM701 20 milligrams per kilogram IV Q4 weeks was identified as the recommended dose for expansion. The expansion cohorts have been initiated and enrolling patients with platinum resistant ovarian cancer, endometrial cancer, and head and neck squamous cell carcinoma. We also reported on preliminary anti-tumor activity and reported stable disease in 3 patients with 1 patient with prostate cancer remaining on study beyond 100 days of treatment. Now moving to Slide 8. We and our partner Bms found the translational data important and noteworthy, indicating Pharmacodynamic activation of the immune system following treatment across P measures, including interferon gamma induction, increased T&N [Indiscernible] cell activation and memory T-cell proliferation at all doses of COM701. This results are significant for several reasons. They are consistent…

Thank you, Henry. Slide 11, please. So far, 2021 has been an eventful year for Compugen, with strong execution across our differentiated clinical strategy, which has solidified our position as leaders in the DNAM axis. As the only Company targeting PVRIG, TIGIT and PD-1 in the clinic, while maintaining our first-mover advantage for PVRIG inhibition in general. And for the three-pathway hypothesis in particular. The strength of this hypothesis has grown through new translational data, which support potent immune activation now also through triple blocade, which is consistent across 2 more types and immune measures. We've also strengthened our deep expertise in PVRIG biology. With preclinical and translational data which support the differentiated profile of PVRIG as an immune checkpoint with exciting data showing increase in activator DC marker in serum of 2 patients is clinically responded to COM701 plus new volume of treatment. This new preliminary observation, suggest that a unique dendritic cells, T-cell interaction triggered by COM701 maybe driving responses in patients and ultimately maybe capable of addressing both inflamed and less inflamed tumor. In the ticket front. Our ultimate strategy is in combination setting and our position is unique in evaluating PVRIG TIGIT [Indiscernible] located in the clinic with our ongoing comp 701 comment of two combination. study. We were pleased to present translational data that support our rationale in choosing an anti-TIGIT antibody with reduced FC effector function, with results demonstrating that comment on to avoids depletion of major TIGIT positive lymphocytes, including CD4 and CD8 T-cells, as well as NK cells, were producing anti-tumor activity on par with other TIGIT assets. We continue to be encouraged by the broad and growing interest in the DNAM space, and our free pathway hypothesis, while also maintaining our first mover advantage and strong IP protection. I'm proud of our execution with multiple key data readouts and the initiation of multiple expansion cohort studies, supported by translational data and with multiple data readouts ahead, which would enable us to take our program forward for the potential benefit of patients. I'm incredibly excited about what's to come, and I'm grateful for the amazing team at Compugen, whose dedication have enabled our remarkable accomplishments. I now turn the call over to Ari to review our financials. Ari.

Thank you, Anat. So, moving to Slide 12. Our financial results for the third quarter of 2021 we did this morning continue to show our strong financial position as we execute across our expanding clinical programs. The $6 million in revenue this quarter, related to the AstraZeneca milestone triggered by the dosing of the first patient in AstraZeneca's Phase 1/2 study of a TIGIT bispecific derived from our COM902. Cost of revenues of $0.7 million are attributed mainly to royalty and milestone payments. Research and development expenses for the third quarter of 2021 were $8.7 million, compared with $5.5 million for the same period in 2020. The increase reflects the expansion and initiation of additional clinical studies during 2021, as well as increased drug manufacturing activities. Net loss for the third quarter of 2021 was $6.2 million or $0.07 per basic and diluted share, compared with a Net loss of $7.8 million or $0.09 per basic and diluted share for the same period in 2020. As of September 30th, 2021, we had approximately $102 million in cash and cash related the accounts compared with approximately $111 million as of June 30th, 2021. With the recent $20 million equity investment by Bristol Myers Squibb, as well as the collection of the $6 million payment from AstraZeneca expected in the fourth quarter. Our year-end cash balance is expected to be in the range of $130 million to $116 million. The Company has no debt. Thank you and with that, we will now open the call for question.

Thank you. Ladies and gentlemen, at this time, we will begin the question-and-answer session. Do you have a question, [Operator Instructions] [Operator Instructions]? Please stand by while we pull for your questions. The first question is from Mark Breidenbach of Oppenheimer. Please go ahead.

Good morning, guys and thanks for taking the questions. I guess I wanted to start with 902 actually, and the dose you've chosen to advance into expansion cohorts. It seems like it's a little bit below what we're seeing used for some of the other TIGIT antibodies, even the fixed dose that the BMS-986207 is being used in your triple study. Could you maybe just comment on why you're confident that you've sufficiently dose-escalated. And you're confident around this 3 mig per kig dose going forward, and kind of what -- the reasons why 902 might be maybe more potent than some of the other TIGIT antibodies that has advanced into the late-stage trials. Thanks.

Sure. Thank you, Mark. And Henry, would you like to start, and maybe Eran will have any additions later.

Sure. I can start. Thank you Mark for the question. So we considered several factors when we selected -- we and the investigators selected the dose that we recommended for expansion, which is 3 milligrams per kilogram body weight IV q 3 weeks. So, one of the things we considered was receptor occupancy, peripheral receptor occupancy. As you know, COM902 is a high affinity TIGIT antibody, so we observed and we've reported in the poster that we achieved peripheral receptor occupancy at 0.1 milligrams per kilogram body weight dose. We also escalated COM902 up through 10 milligrams per kilogram body weight dose and the overall recommendation from review of the data, including the PK data, was that we didn't think in addition with the investigators and the authors on the study, that going beyond 3 milligrams per kilogram body weight dose was going to add anymore clinical benefit in terms of the outcomes for the patients. So that's the reason we selected 3 milligrams per kilogram body weight dose. Now, when you benchmark that dose and you compare it to what the periphery receptor occupancy is, that's at least a margin of 30. That's significant enough to have tissue penetration in the tumor micro-environment. I wouldn't want to comment on the metrics for other companies, but I think if you go back and look at the way they've demonstrated their receptor occupancy and selected dose. It's very similar across companies. So, we're not, we're actually in the mainstream.

Maybe just to add. When did we compare COM902 to the other leading TIGIT benchmarks? And indeed, COM902 has better binding, better blocking, and at least as good or better functional activity in vitro. We're glad to see to be translated also into achieving full [Indiscernible] occupancy in a relatively low level compared to the other published data. And yes, as Henry mentioned, we believe that this dose that we chose is would be sufficient to allow for full-year occupancy also in the tumor micro-environment.

Okay. And just with respect to that one Grade 3 atrial segment is this a toxicity that's been seen in other studies of TIGIT antibodies, is there any chance in your mind that this is a class effect or you think this is a one-off?

Yes. So Mark it's a good question. We think it's a one-off for several reasons. So, we will come back to look at the pre -clinical data. We have repeat dose toxicity studies that were conducted prior to initiating the human experiments, the human clinical trials that we have. And the repeat dose toxicity studies did not demonstrate any EKG findings as I noted in my prepared comments. In addition, we didn't actually see -- we didn't see any additional toxicities when we escalated through 10 milligrams per kilogram body weight dose like I said in my prepared comments. Now that particular patient, I can give a little bit of more information. So, the patient came in, had -- was diagnosed with atrial fibrillation, and that resolved on the same day that the patient came in. This was about a week through the first dosing interval in the first cycle. So, we think it's a one-off effect. Now, we do not know if the other companies that have TIGIT inhibitors report all the data. So, you can imagine that sometimes the data that is reported might be limited to maybe 3 patients or 2 patients, and the single-digit toxicities may not be demonstrated. But we don't think based on preclinical data that this has any bearing or any relationship to COM902. That's our assessment.

Okay. Thanks for taking the questions. I'll jump back into the queue.

The next question is from Stephen Willey of Stifel. Please go ahead.

Good morning. Thank you for taking the questions. Maybe to follow-up on COM902. I think the lack of lymphocyte depletion on TIGIT positive cells is interesting, but can you remind us what is the magnitude of decrease that you would expect to see in these cell subtypes with those TIGIT antibodies that have been engineered to have enhanced effector [Indiscernible]

Yes. So, some of the companies did publish these results. And what they have shown is dramatic reduction, is not like a minor reduction, it is in peripheral blood. As we all know in tumor microenvironment, the depletion normally is much more challenging, so we don't know if there is any kind of depletion tumor microenvironment. When peripheral blood, they have shown depletion of CD8 positive -- TIGIT positive cells in the peripheral blood. And that the reduction was dramatic.

Okay, that's helpful. And then on the triple combo biomarker data that you have again, I guess it appears to support the hypothesis that PVRIG is contributing something. But I know the way that the data is presented, it's a function of all doses. Is there anything that you can say with respect to their potentially being a dose dependency to some of these changes in biomarkers that you're seeing as a function of escalating COM701?

Okay. So, in this trial in the treatment study, the dose response range was not as big as we had in the past, so absolutely started in 1 patient in all 3 and then already moved to 1 make per kick which is the already 4-step that you can see. So, in this specific context, we haven't seen much of a dose response. I reminded in the past and we had provide a range of responses, concentrations we did see a dose response of COM701 and combination with nivo etc.

And maybe you can just lastly, talk about, how the expanded Bristol collaboration, intersects with the fact that you are now through dose escalation with COM902. You're going to be interrogating various combinations with that agent. How do those two things overlap with each other if at all? And are you guys, I guess on the guardrails in place embedded within the collaboration such that your kind of each day in your own way.

I relate to that, Steve. So, this collaboration -- actually this expansion of the collaboration reflects on the long-term -- long-standing relationship between the 2 companies. It is -- it stands for itself. It is really designed in order to enhance the strategic collaboration. It is enhanced -- it is designed to support the kind of studies that we have, to support Compugen in executing these studies. At this point in time, we are on the packaging front of -- on the clinical strategy front. We are at the stage that we completed all the dose escalation studies that we wanted to do. And we already started the expansion cohort. And remember that we have with Bristol now. Two combination studies. The consequently, volumes hub and the triplet. And each of the study is conducted in multiple tumor types. We have broadly translational program that this with PD markers and immunohistochemistry, as we stated in the past also, we're trying invest technology on our patient-center. So, the collaboration is actually growing and growing, and both parties felt that it would be good to have a Joint Strategic Oversight Committee that is actually working in parallel to the Joint Development Committee that is working at the operational level. At this point in time, having all studies being expanded, that's the right time for us to align on the strategy of how we're interpreting the data together, and how we think about next step.

All right. Thanks for taking my questions.

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

Hi. Thank you for the question. And congratulations on the data, guys. I wonder first on COM902, if you could give us any more details about the nature of these stable diseases. Did you see tumor shrinkage? Was there's not so much shrinkage and a lot of stable. Any notable case studies that gave you a lot of confidence.

Thank you very much for the question, Daina. We did look at the metrics for the patients that were enrolled. We, with the investigators, considered that we had enough data embedded in the poster to inform the clinical profile of the subjects -- of the patients that were enrolled on the study. So, the things that we were focused on, essentially, were looking at the treatment journey or the course of the patient, so -- which is illustrated in the [Indiscernible] plots. We think that the [Indiscernible] plot best represents how heavily pre -treated those patients were. We also provided icons in the [Indiscernible] to illustrate the patients who had received prior immune checkpoints and patients who had prior treatment refractory disease. So, one of the other things that we look at as based on enrollment on the study, was that for patients who are in dose escalation and its only dose escalation that we're reporting, the assessment of measurable disease is not an eligibility criterion. So, we didn't think that would inform on whether patients had tumor reductions. Yes, patients could be evaluated based on resist but we thought that the most appropriate way to illustrate the anti-tumor activity of COM902 was to demonstrate this by the [Indiscernible] Yes, we did see a few patients with tumor regressions, but if you look carefully at the swimmer plot, I think it best answers the question of how patients were doing on the study. And that's why we decided to just go with the swimmer plot.

A follow-up then. So how many of these patients or do you know -- I don't see the notation. Which of these patients started with measurable disease and which ones did not?

Yeah, we decided not to include that because -- since it was not an eligibility criteria, not a lot of the patients had measurable disease. And we wanted to convey the finding of the anti-tumor activity, including confirmed stable disease that we demonstrated in the [Indiscernible] So if you see the -- on that [Indiscernible] We have of the 18 patients, 9 of them with either best response assessment of stable disease, and out of this 9, 2/3, 67% with confirmed stable disease. And of course, 3 patients with stable disease that's 6 months or longer. The icons that we illustrate in the [Indiscernible] I think provides a surrogate assessment for how COM902 as mono-therapy through those escalations has some form of clinical benefit for the patients that are enrolled. So, I think it probably, if you think very carefully about it, it provides you with the enough information on how patients are doing on the study.

Okay. Maybe one more follow-up. For the patients of prior immune checkpoint inhibitor, do they follow, let's say the 50 guidelines, for washout of between the periods that confirmed progression on the checkpoint.

Yes. We had certain benchmarks in the protocol with regards to eligibility for enrollment onto the study. Of all the patients that we had out of those 18 patients we enrolled, 8 of them had received prior immune checkpoints. And we -- if you look at the [Indiscernible] plot, it best illustrates those patients that I can just go through them. So, we had a patient with a [Indiscernible] I don't know existed carcinoma, peritoneal cancer, small cell lung cancer [Indiscernible] prostate cancer, renal cell carcinoma and caustic cancer. Yes, we follow the guidelines In terms of wash out.

Perfect. okay. Thank you very much.

No worries.

The next question is from Chris Howerton of Jefferies. Please go ahead.

Hi. Good morning. And congratulations on the progress and really appreciate you taking the questions. I think a lot of really good ones have already been asked, but maybe just 2 from me. One would be -- could you comment at all on any safety that you've seen with respect to the triple combination study? Any notable toxicities or things that would suggest things like immune activation or things like CRS would be one question. And then the second question that I would have is, this might be a little tougher to think about, but one of the things that's notable about the patient populations that we have here is that they're heavily pretreated by 10 -- medium line of 10 previous therapies. So how can we think about the potency, certainly of 902, in the context of patients with the healthier immune system, and what are some of the things that you're going to be looking out for as you move forward in that context? Thank you.

Maybe I can start. So, in terms of cytokine release syndrome, we didn't observe this. None was reported on the study for the triplet and also for COM902. This was not something pre-clinically that we thought we will see. And so far with the reports that we have, we haven't reported this, neither have the investigators. Even though they asked this questions and do the lab work on the patients, as reported or observed is also. We think that based on the mechanism of action of COM902, and also as part of the triplet, that the toxicities that we've observed, toxicities that are not unique highlight to COM902, or the toxicities that are unique as part of the triplex. You know that we have accumulated a lot of data on COM701. So let me speak about the triplet first, on COM701 as mono-therapy, and we can say, categorically, that it is very well-tolerated as mono-therapy, and it has a favorable safety profile. We also have enough information at this time with regards to COM701 in combination with nivolumab, which we'll disclosed at ASCO. It is also well tolerated and has a very good safety profile also. We did not observe any of these toxicities that you mentioned. The most frequent toxicity observed as monotherapy for COM701, in combination also with nivolumab and also as part of the triplet is fatigued. And it's typically grade 1 or 2 fatigue that we've been able to show. The other toxicities that we've seen in combination, are things that are constitutional in nature and related to the cancer that the subjects have. Either they have elevated liver function test abnormalities as a result of progression in the liver, or they have obstruction of certain organ components because of the prevailing cancer itself. So, there's nothing that is unusual in the studies that we've seen so far. For COM902 specifically, it's very well-tolerated also. Mark asked about the patients with atrial fibrillation, we think it's a one-off based on the preclinical data that we have. We didn't observe sacroiliac syndrome in that. Also, we did note that in addition to most of the patients doing well on study treatment, only one subject came off, and that's -- this subject that had the treatment discontinuation that we'd describe. That's the patient with prostate cancer with atrial fibrillation, that I mentioned. So, I'll stop there.

Okay. Alright then. That's great. Thank you very much, Henry.

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

Yes, thanks very much. The question or series of questions. One is, in the triple study, small number of patients, but what is considered a high expresser of PVRL2? That's question one. And then question 2, two parts. Going back to the translational data, which I have a lot of respect for. A question was actually asked about dose response. But I am curious about the pharmacokinetics of 701 and especially given the low dose versus high-dose. And importantly, is there any correlation to dose level and duration, that's part A. And then B. Do you have a hypothesis as to why, if in fact, I realize that the translational data is all peripheral? We don't really know what dose on at the tumor site unless you have a view about that. But what's really -- why don't we see greater tumor shrinkage. And it may be simply because these are very, very sick patients. They've had multiple therapies, I'm respectful of that. I'm just curious of your hypothesis on that point. Thanks very much.

Okay. Thanks. I think I can take it. So first of all, for the high expressor of PVRL2, as you may remember, we published quite extensively in the past that certain tumor types have higher expression of PVRIG and PVRL2. And these are the indication which we're moving forward to now. So just indication which PVRL2 in terms of age score, if you wish, it's probably 200, 300 atleast for the first one. Then for the dose and duration, Henry, you probably want to take this one and I could take the third one.

You're correct that the duration is a reflection of the heavy pre -treatments that dictations on the studies we're on. Just as a matter of fact, we did indicate that in our prepared comments and also on a poster that in median of ten prior therapies with a range of one through 19, and if you think of the COM701 nivo study, this was immediate of five. So, it's actually essentially a doubling of the media anti therapies. If patients unable to stay as long, then you probably will not be able to see this correlation that is of interest to you, that is also of interest to us. So, it's all based on the heterogeneity of the patient population, and the length of time patients stay on. Those are the key metrics that inform on the relationship with treatment outcome.

And then for the third one. So [Indiscernible] translational data. So, we're very excited about this data, and also partnering with BMS. We're studying this pathway for over a decade. And we established the biology and established the preclinical data that shows that if you combine the 3 agents together, they're all modulating DNAM axis, and they eventually are synergistic in multiple models in the clinical settings. And now for the first time we see, in patients, such a potent [Indiscernible] reflected by the potency, by the consistency, and evidence by multiple [Indiscernible] And this is very exciting, to see this transit now into patients. Now in order to actually see, and maybe just to mention again, as mentioned before that if you compare this data to our own data with COM701 on mono NN combination, and also to all published data that we're aware of, of TIGIT and mono and combinations, the effects still seem again more and more robust and more potent, again suggesting that the triplets are doing something different from each of the combination of the agents by themselves. Now, what about the tumor microenvironment. As mentioned, these are heavily, heavily pretreated patient population in this specific trial. And more things need to happen if your macro environment in order for the actual see tumor shrinkage. So, where we have 4 [Indiscernible] and also biopsies and want to expand the trial and also look at your micro-environment. This peripheral immune effects are potent and probably in these heavily pre -treated patient population we're not sufficient into macro-environment to modulate it enough to media tumor shrinkage. And we are looking forward to see how will this regime look like in our above-market driven approach in the expansion towards.

Excellent am grateful. Thank you very much.

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

Hey, good morning, guys. Thanks for taking the questions. I guess just starting off with the triplet and Henry, some of the comments you have made regarding the extension cords. Did I hear right that prostate wasn't one of the ones that you will be expanding into and if I did hear right, I was just kind of curious given the long-standing SD that you have here, why that is.

Thank you. Reni. So, for the expansion cohort, for the triplet, we're focused on the biomarker informed patient population. So, we're focused on ovarian cancer, we are focused on endometrial cancer, we're also now focused on head and neck squamous cell carcinoma, and we also have a basket cohort. This is of interest to us also, prostate cancer. But understandably, we think we need to prioritize the indications that are of interest to us. And that's why we're focused on what we have now currently at start of the expansion for the triplet.

Okay. And then as you guys have looked at this data, has there been any new biomarker-based insights that you might be able to provide more color on. And have you learned anything new that you might be able to expand -- where you might be able to use in your expansion cohorts?

So, I would say that again, the main observation is just mentioned that the [Indiscernible] and prefer blood. Regarding biopsies, they are not mandatory in this part of the trial, but obviously this is work in progress. We are collecting samples for all the patients, especially knowing the expansion cohorts will follow with correlation to different biomarkers we explore, will explore also modulation in the 2-macro environment. But this is all work in progress.

Reni, I just --

Sorry. Go ahead, Anat.

I just -- I'm just going to say that in general, and Eran was alluding to the fact that we were observing potent immune activation in the triplet, in the doublet, in -- with COM701 alone. From our perspective, it is really high supportive, the hypothesis that we came up with for the PVRIG pathway, and in combinations. And that for us was critical in the dose escalation setting just to get more comfortable entering into the expansion cohort. But now, there's a lot of work ahead of us. Pushing these studies forward and making sure that we act on all fronts on that translational approach that we're taking together with evaluating the [Indiscernible] at this point in time this is what we have, but we are encouraged with this.

Got it. And I guess just finally, given these results in the triplet and how happy you are with them, why not evaluate 902 and 701 with an additional either PD-1 or PDL-1 inhibitor versus the ongoing 902, 701 studies, And when we think about PD-1 versus PD-L1, right? If we look at Roche's data, it's -- you see that response rates with the PD-L1 inhibitor. Is there a biological rationale why to stick with, let's say, Opdivo? I understand from a cost perspective and the Bristol collaboration, but is there a thought process or something that you guys are thinking about now where you might want to evaluate some other combination partners. Thanks. Thanks'.

On AstraZeneca dose Henry if you have any additional [Indiscernible] in. And we're now -- we've now launched the studies that we wanted to do, and we're doing it in preparation with Bristol-Myers Squibb and we use nivolumab. From my perspective, obviously, these studies are serving as a way for us to try and address the relevant and drug combinations for the different patient populations in the different indication. And try to assess which indications and combinations we should focus on. For the future study. Having said that, we're not ruling out using additional PD-1 /PD - L1 inhibitors in the future. At this point in time, under the collaboration with BMS, we're committed to pursue this path forward, and get the data that we need in order to dive more deeply into certain indications with certain combinations. Henry, do you want to add anything.

I think you've said most of it. Just one little part of it that I think you've articulated very well before in the past, and continuously, Anat, and that's not just to look at the PD-1 / PD-L1 access, but also to rely on the strength that Compugen has with its antibodies. We also think strategically of a PD-1 and the PD-L1 free regimen. And as a consequence of that, we have this ongoing study with an expansion cord of COM701 and COM902 and learning patients with non-small cell lung cancer, head and neck squamous cell cancer, and also colorectal cancer. So that's the other strategy, which I think might be of interest to you also. And I know you remember these, Reni, so not just the PD-1, PD-L1 combination, but one that is free of those agents.

Great, thanks for taking the questions.

This concludes the Q&A -- there is an additional question. The next question is from Asthika Goonewardene of Truist Securities. Please go ahead.

Thanks for taking my questions. My apologies [Indiscernible] of background noise where I'm up employed, city here. I just wanted to check on the patients -- on the triplet combination, that you did show stable disease. If we're able to get any biopsies of the tumors on progression. And maybe can you talk just a little bit about what were the signals that you might have been seeing that been driving the progression after the therapy. Thanks.

Yeah. I think that's a good question. So, for patients, because it's Dave that we're presenting, is that dose escalation biopsies not mandatory, as opposed to patients were enrolled on the expansion cohort where they ease pre assessment with a biopsy and another biopsy after a certain number of periods of time on the study. So, the short answer is, we do not have [Indiscernible] on any of these subjects. one subject to the other ongoing or the subjects who had stable disease or the subjects to progress.

Great. Thanks for taking my question, guys.

This concludes the 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 for joining us today and your continued support. We hope to save your safety. Stay safe and healthy.

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