Compugen Ltd (CGEN) Q2 2021 Earnings Call Transcript

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Compugen Ltd (CGEN 4.76%)
Q2 2021 Earnings Call
Jul 28, 2021, 8:30 a.m. ET

Contents:

• Prepared Remarks
• Questions and Answers
• Call Participants

Prepared Remarks:

Operator

Ladies and gentlemen, thank you for joining us today. Welcome to Compugen Second Quarter 2021 Results Conference Call. [Operator Instructions] An audio webcast of this call is available in the Investors section of Compugen's website at 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 Naughton -- Head of Investor Relations and Corporate Communications

Thank you operator and thank you for joining us on the call today. Joining me to present prepared remarks are Anat Cohen-Dayag, President and CEO; and Ari Krashin, CFO and COO. For the Q&A session, we will also be joined by Henry Adewoye, CMO; and Eran Ophir, Vice President, Research and Drug Discovery. Before we begin, I would like to remind you, that during this call, the company may make projections or forward-looking statements regarding future events or business outlook; our development efforts and their outcome; our discovery platform; anticipated progress, results and timeline for our program; financial and accounting related matters; as well as statements regarding our cash position.

Such statements represent only on the company's current beliefs, expectations and assumptions, while actual results, performance or achievements of the company may differ materially. These statements involve known and unknown risk and uncertainties, and we refer you to our SEC filings for more details on these risks, including the company's most recent report on Form 20-F filed on February 2021. The company undertakes no obligation to update projections or forward-looking statements in the future.

With that I will turn the call over to Anat.

Anat Cohen-Dayag -- President and Chief Executive Officer

Thank you, Yvonne. Good morning, and good afternoon, everyone and welcome to our second quarter 2021 update. Our continued progress through 2021 has been strong with steady execution, solidifying our leading position in the genome access and differentiating us in the TIGIT space as the only company targeting in a clinical setting PVRIG TIGIT and PD-1 as part of our three pathway hypothesis. On today's call I'm pleased to have the opportunity to remind you of our strategy, provide perspectives on our most recent data, our views on important developments in the field and what's to come for the remainder of 2021.

We believe that the foundation that underlies our success as Compugen is our science and our people. We were the first to identify PVRIG IL-02 as novel checkpoints and we published on TIGIT, the same year as Genentech. Both PVRIG and TIGIT are key pilot and complementary inhibitory pathways in the genome access which also intersect with the well-established PD-1 pathway. While TIGIT and PVRIG pathways share similarities, we observed key differences between the two with respect to their expression pattern and their [Indecipherable] expression pattern on immune cells and tumor types.

Furthermore our recent data shows that PVRIG is expressed similarly to PD-1 and TIGIT in stem cell like memory and exhausted T cell, an important cell population with the potential role in mediating antitumor effects. However recently, Eran Ophir, our VP of Research and Drug Discovery presented scientific data showing that PVRIG has a more dominant expression pattern on early differentiated stem like memory T cells than TIGIT and PD-1 further pointing to the possibility that PVRIG may act differently. We believe that the future of immuno-oncology will be driven by combination approaches. Research from Compugen suggests that the PVRIG TIGIT and PD-1 pathways have different dominance in different to more types and patients implying that to induce effective anti-tumor responses certain patient populations may require the blockade of different combinations of these three pathways.

To test this hypothesis Compugen has established a biomarker and biology informed clinical program which aims to evaluate different combinations of this axis members across tumor types. We're focused on maintaining our first mover advantage in the clinic the only company with monotherapy doublet and triplet combination clinical studies evaluating the DNAM axis PVRIG and TIGIT as well as PD-1. We believe this programs anchored by our first-in-class anti-PVRIG antibody COM701 uniquely position Compugen with innovative and potential first-to-market doublet and triplet therapies. Our most recent data from the Phase 1 dose escalation and expansion cohorts of COM701 as monotherapy and in combination with nivolumab presented at ASCO this year are important for several reasons.

These preliminary data showed durable responses and disease control in patients who exhausted all prior treatment options which may have meaningful effect. Notably these responses were in two more types typically in not responding to immune checkpoint inhibitors. COM701 in combination with nivolumab resulted in a disease control rate of 67%. This included a complete response in a patient with anal squamous cell carcinoma who had prior treatment with nivolumab and departure response in a patient with microsatellite stable colorectal cancer. These are two more types typically unlikely to respond to checkpoint inhibitors and at the time of reporting, we saw responses up to and beyond one year.

Moreover, our potential differentiation comes through the addition of an anti-TIGIT antibody to this doublets regimen in our ongoing triplet combination study and combining anti-PVRIG with anti-TIGIT in our newly initiated anti-PD-1 independent study. These data are also important as they demonstrate signals of anti-tumor activity in a COM701 monotherapy setting in patients who have exhausted all available standard therapies and in tumor types typically not responding to immune checkpoint inhibitors. COM701 resulted in a disease control rate of 47% including one partial response. It is also important to note that COM701 was well-tolerated with no DLT with monotherapy or in combination with nivolumab.

This is a critical component of our ability to move forward with our differentiated combination approach. This preliminary data are also important as they included our first initial pharmacodynamic biomarker data which indicated treatment with COM701 leads to immune activation. We also showed that antitumor activity was observed in selected PD-L1 low, PVRL2 positive patients, suggesting COM701 treatment may drive antitumor immunity even in patients with less inflamed tumor microenvironment, I will come back to this data and a broader biomarker strategy later in the call. Competent execution in the clinic has been impressive.

In a short time we have gone from our first clinical launch and data presentation to a comprehensive clinical program with the opportunity to truly differentiate us in the genome and TIGIT space including the ongoing cohort expansion of COM701 in combination with nivolumab, the triplet study of COM701 with nivolumab and Bristol Myers Squibb TIGIT inhibitor for which we just announced initiation of the cohort expansion study. The dose escalation of COM902, our wholly owned TIGIT Inhibitor and the recently initiated doublet study of COM902 and COM701 initially evaluating the safety and tolerability of the combination at both of the recommended doses for expansion in patients who have exhausted all available standard of care therapies, i.e., all comers.

Once this is completed an expansion cohort of both study drugs will be initiated in patients with PD-1 refractory or relapse non-small cell lung cancer and head and neck squamous cell carcinoma as well as colorectal cancer, microsatellite colorectal cancer. Having completed the dose escalation of the triplet study and initiated the triplet cohort expansion study, we continue to evaluate strategies to maintain our fast execution and first mover advantage. We are considering removing randomization from the variant arm of the triplet study, as historical data for nivolumab in ovarian cancer already exist and we know these patients have low response rate to nivolumab.

In addition, we are considering adding an inflamed indication possibly head and neck cancer to broadly assess the full blockade of this access in a tumor type death, unlike most of the other tumor types we evaluate has an inflamed histology but still presents a low response rate to immunotherapies. And finally our plan for the triplet includes starting the basket study when we have additional data aiming to support the link between PVRL2 expression and treatment response. Coming back to our biomarker strategy, on which we receive a lot of questions, I thought I would take this opportunity to summarize our approach.

Firstly, we use biomarkers to select the tumor types for inclusion in our cohort of expansion studies. This was driven by our computation of discovery prediction, and validated in the lab on DNAM axis members expression in tumor samples, along with our initial clinical results from the dose escalation studies of COM701. Our focus in the various expansion cohort studies we initiated is on two more types with a high level of both PVRIG and PVRL2 and the two more types in which we saw initial signals to antitumor activity in the dose escalation studies. Such antitumor activity further supports our biomarker informed approach and predictive discovery capabilities.

The second part of our biomarker strategy is the identification of biomarkers for future patient selection. To achieve these goals we are currently evaluating the correlation between the expression of the PVRIG pathway with clinical response as well as other exploratory biomarker identification approaches. This work is being done in our ongoing court expansion studies in which tumor biopsies are collected pre and on treatment. And thirdly we have a pharmacodynamic biomarker approach where we measure immune modulation induced by COM701 in combination in peripheral and tumor patient centers obtained before and during treatment as mentioned earlier.

Our first presentation of our preliminary biomarker results at ASCO provided initial clinical evidence for the potential immune mediated mechanism of action with COM701. After one treatment cycle patients with COM701 monotherapy showed the trend of increased proliferation of a sector memory CD8+ T-cells. This is an important cell population particularly given its high expression of PVRIG, enrolling driving antitumor activity. In addition we saw a significant proliferation of NKT cells which also plays a role in anti-tumor activity.

From a cytokine perspective levels of interferon gamma cytokine that plays a key role in anti-tumor activity were upregulated following combination treatment of COM701 plus nivolumab. Interestingly these results showed a dose response trend with increasing doses of COM701 and fixed doses of nivolumab suggesting that you observed increasing cytokines is derived from the combination regimen and not nivolumab alone. We're excited to present a case study at ASCO which included archival biopsy data patient with platinum resistant MSS primary peritoneal cancer. This patient with a confirmed PR who was on treatment for 18 months was PDL-1 negative prior to treatment with PVRL2 expression on both tumor and endothelial cells and an immune desert phenotype.

Peripheral blood assessment in this patient showed immune activation as measured by immune cell proliferation and in different gamma induction prior to two more shrinkage. This biopsy and peripheral blood biomarker case study together with our recent finding of PVRIG expression profile on stem cell like memory T cells and each ligand on dendritic cells suggest a potential mechanism of action of COM701 in driving tumor shrinkage Likely through immune activation in a patient with an immune desert non-inflamed tumor microenvironment. These immune desert non-inflamed patients are those who are typically considered least likely to respond to checkpoint inhibitors.

And we're encouraged by these initial results which provide the first translational indication, that targeting the DNAM axis may expand the reach of immunotherapy to patients who typically do not benefit from these treatments. Our steady execution over the past year has propelled us to a unique first mover advantage as the only company with wholly owned clinical stage assets for both PVRIG and TIGIT. Recent developments in the field are providing important validation of our freeway hypothesis with considerable interest growing in pursuing similar approaches in evaluating the dual and triple blockade of genome access members, PVRIG and TIGIT along with PD-1.

We believe that growing interest in the field endorses our overall strategy from target discovery and validation through to our clinical strategy. And while others are looking to advance candidates targeting PVRIG into clinical studies, we remain ahead with clinical evaluation of monotherapy, double and triple combination regimens already in progress with COM701. A part of the growing interest in the genome access includes a debate regarding the role of the FC domain and its relevance for antitumor activity for immune checkpoint inhibitors in general and TIGIT antibodies specifically.

And while the debate for TIGIT antibodies is ongoing, which was a point of discussion at the recent SITC Symposium on TIGIT. The consensus is that it is unclear if pre-clinical results from mice or in vitro studies support Fc active TIGIT antibodies will translate to the clinic. COM701 and COM902 were both purposely designed by Compugen to have reduced Fc effect of function as we believe this best positions us for success in the clinic. Antibodies with Fc effect of function carry the risk of depleting CD8+ T cells which are crucial for driving anti-tumor activity in the solid tumor setting.

Our strategy is to avoid the risk of depleting these important cell population and our growing data support this decision with preliminary activity in the clinic with COM701. In addition the recent developments in the field indicating promising Phase 2 randomized descriptive data within Fc silent anti-TIGIT are in line with our Fc reduced function approach. So far 2021 has been a year of execution for Compugen and we plan to continue this execution through the second half of the year with several milestones still expected to come.

Among these milestones, will be preliminary data from our leading Phase 1/2 triple combination study evaluating the safety, tolerability and preliminary antitumor activity of COM701 in combination with Bristol-Myers Squibb TIGIT antibody and nivolumab. We remain on track to report initial data from the study in the fourth quarter of the year We remain on track to report initial data from this study in the fourth quarter of the year which tests our triple blockade hypothesis that blocking the three intersecting PVRIG, TIGIT and PD-1 pathways has the potential to synergistically enhance anti-tumor immune responses in selected patient populations not responsive or refractory to PD-1 blockade.

This is a key differentiator for Compugen in the competitive TIGIT space. Our progress with a triple combination study continues with a recently announced initiation of the expansion cohort of this study. Moving next to COM902. The COM902 monotherapy dose escalation study is important as it enables us to select a dose to independently evaluate multiple combination approaches with COM902 in the clinic. We expect to provide initial data from the COM902 dose escalation in the fourth quarter of this year. We also strengthened our track record of executing in the clinic with the on-schedule initiation of our clinical study of COM902 in combination with COM701.

This study is the first clinical evaluation of the dual blockade of PVRIG and TIGIT is again a key differentiator for Compugen in the competitive TIGIT space. As we know, we also have an ongoing collaboration with Bayer and we are pleased with their commitment in advancing our ILDR2 program. Like PVRIG, ILDR2 was first discovered by Compugen. Bayer have full responsibility for development of the bapotulimab, which is a novel first-in-class anti-ILDR2 monoclonal antibody. We're pleased to be able to say that enrollment is accelerating in the Phase 1 cohort expansion study which is focused on treating patients cohort expansion study which is focused and treating patients with first line IO naive head and neck squamous cell carcinoma.

We look forward to sharing additional updates on the progress of this collaboration in the future subject to Bayer's communication policy. We're proud of our remarkable progress, excited for what's to come and remain committed to pioneering the science and clinical studies that have the potential to expand the reach of immunotherapies to patient populations who are unresponsive or refractory to current treatments. Before turning the call over to Ari, I would like to thank the team at Compugen, our partners, investigators, shareholders and patients. I am incredibly proud of their ongoing commitment and dedication which has enabled our impressive execution.

And with that I will turn the call over to Ari to review the financials.

Ari Krashin -- Chief Financial and Operating Officer

Thank you, Anat. Good morning and good afternoon to everyone. Our financial results for the second quarter of 2021 released this morning continue to show our strong financial position as we execute across our growing clinical programs. Research and development expenses for the second quarter of 2021 were $6.8 million compared with $4.4 million for the same period in 2020. The increase in expenses reflects the continued execution and expansion of the various clinical trials Phase 1 programs.

Net loss for the second quarter of 2021 was $9.5 million or $0.11 per basic and diluted share compared with a net loss of $6.2 million or $0.08 per basic and diluted share for the same period in 2020. As of June 30, 2021 we had approximately $111 million in cash and cash-related accounts compared with approximately $119 million as of March 31, 2021. The company has no debt. As a reminder we expect our gross cash expenditures for 2021 to be in the range between $40 million to $42 million without taking into consideration any potential cash inflows for the company from existing and new collaborations.

Thank you. And with that we will now open the call for questions.

Questions and Answers:

Operator

Thank you. [Operator Instructions] The first question is from Mark Breidenbach of Oppenheimer. Please go ahead.

Mark Breidenbach -- Oppenheimer & Co., Inc. -- Analyst

Hey. Thanks for taking the questions and congrats on the progress. So let me maybe start with a kind of science you've won. We certainly appreciated Eran's presentation showing the fraction of TCF7 positive cells is important for response to checkpoint therapy, and that there's expression of PVRIG in stem-like T cells. I guess I'm wondering if you see TCF7 as a potential biomarker for patients who walks in, would you expect there to be many patients in your Phase 1 dose escalation trials who still have stem-like T cells? And is that the kind of thing that can be simply monitored from peripheral blood without needing biopsies?

Eran Ophir -- Vice President, Research and Drug Discovery

Yeah. Thanks Mark. So I think it's an interesting notion, which is not relevant only to PVRIG but to the field at all, the expansion of TCF1. I think its might be challenging biomarker in terms of its prevalence, an expression in TME but we are looking in addition to the obvious aspects in DNAM pathway, etc. We are looking quite broad in terms of exploratory biomarker identification, obviously, TCF7 is one of them and peripheral blood, I'm not sure it's correlated enough the presence of the cells in blood compared to tumor.

Mark Breidenbach -- Oppenheimer & Co., Inc. -- Analyst

Okay, fair enough. And just in terms of what we should be expecting as far as patient numbers for the upcoming readouts in -- from the triple combination dose escalation study and COM902 monotherapy dose escalation study and also might we see additional kind of translational biomarker data compared to archival biopsies for any of these patients or will the focus really be more on safety and efficacy in the fourth quarter?

Anat Cohen-Dayag -- President and Chief Executive Officer

So just, I'll let Henry relate to it but just for the translational data, we're accumulating data, we're working on translational data generation from our studies. When we will have the data, we'll present, not sure that this will be ready for the Q4 or maybe we'll have only very initial data. And as for the expectations, I'll let Henry relate to it.

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Yeah. So it'll be along the -- Mark, thank you very much for your question. It'll be along the same lines of the subjects that we were previously enrolled in dose escalation, so an approximate range would be between the strength of 15 to about 20 patients for the dose escalation.

Mark Breidenbach -- Oppenheimer & Co., Inc. -- Analyst

And that's for both the triple combination and for COM902 as well?

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Yeah, that is correct, Mark.

Mark Breidenbach -- Oppenheimer & Co., Inc. -- Analyst

Okay. Thank you so much for the clarification and thanks for taking questions.

Operator

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

Chris Howerton -- Jefferies LLC -- Analyst

Excellent. Thank you so much for taking the questions. And of course congratulations on the progress and look forward to the end of the year here. So maybe just a couple of questions from me. One is maybe just more of a theoretical question in terms of some of the checkpoint axes, obviously, the DNAM axis is the focus for your team, but there's also been some activity with VISTA in the associated macrophage lineage. So I guess I'd be curious to hear your thoughts on how those may or may not synergize or work together. I mean, then the second question I have is I know Anat, you were mentioning around the good strategy and the hypothesis is that you have around the Fc domain of your antibodies. There was a recent update from Arcus. Obviously, a little scant on details but curious to hear your thoughts as to how that reads through to your programs. Thank you.

Eran Ophir -- Vice President, Research and Drug Discovery

Okay. Thanks Chris. For first -- for your first question, not sure what business specifically, but if you're talking about MIALU checkpoints in general, this is something we entered few years ago. Yes, we do think that MIALU plays an important role in immune suppression in tumor microenvironment and we have early programs on this -- in this front. And we are evaluating, of course, efficacy in combination, its synergies with current pipelines, assets, etc.

Chris Howerton -- Jefferies LLC -- Analyst

Okay.

Anat Cohen-Dayag -- President and Chief Executive Officer

And for the...

Chris Howerton -- Jefferies LLC -- Analyst

Go ahead. Sorry.

Anat Cohen-Dayag -- President and Chief Executive Officer

Yes, no, I just wanted to add for the Fc domain question and the Arcus data. So obviously, we were not surprised to see this descriptive -- data positive descriptive data. We're waiting to see the data itself. But remember that this is an approach that we were taking ourselves and we believe in this approach, we selected an IgG4 purposely. So it was encouraging for us to see that we were expecting it.

Chris Howerton -- Jefferies LLC -- Analyst

Yes, OK. And then maybe if I may just one other quick question with respect to kind of the tumor microenvironment that you're describing like head and neck where it was inflamed but not necessarily responding to immunotherapy. I guess what is the mechanistic hypothesis there in terms of specifically what the checkpoints are and how is it inflamed, yet no appreciable immune response to the actual tumor?

Eran Ophir -- Vice President, Research and Drug Discovery

So we're moving in few fronts, evaluating few different hypotheses, the -- as discussed in the script, the expression of PVRIG in stem-like T cells, the expression of PVRL2 in dendritic cells, all of this make us think that PVRIG may be a dominant checkpoint in terms of enhancing T cell priming, expansion and thereby enabling targeting also patients have less inflamed tumor microenvironment and we presented in ASCO preliminary data to show that we see some early signs of antitumor activity in patients, which have a PD-L1 low less inflamed tumor types.

But obviously, every check when should work better in a more inflamed tumor microenvironment because the T cells are already there. So you might need to push it a bit less to get the efficacy and two most like head and neck and even other more inflamed might also have a potential for PVRIG, in terms of enhancing and expanding the T cells which are already these, releasing another break that might be the one which is relevant if PD-1 alone is not itself and head and neck, and non-small cell lung and other hotter indications have a quite dominant expression of the pathway of PVRL2 and others. So I think that we are testing in a clinical strategy, multiple indications, which fits different while hypotheses all stemming from the same biology of PVRIG and PVRL2 and the role in T cell expansion.

Chris Howerton -- Jefferies LLC -- Analyst

Yes. Okay. No, I get it. Okay. Thank you very much, Eran and appreciate you taking the question.

Operator

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

Reni Benjamin -- JMP Securities -- Analyst

Hey, guys. Thanks for taking the questions and congratulations on all the clinical progress. I guess just sticking with the TIGIT theme, we've seen some significant BD activity most recently, I guess with BMS and Agenus. And I just wanted to get your thoughts as to, I guess, how we should be thinking about your own BD discussions and your thoughts regarding the potential to partner or is there something that you really want to keep in-house? And sticking with the TIGIT theme, when I think about, I think, I know you had made some comments about how the strategy with having a inactive or slightly less functioning Fc effector prevent CD8 T cell depletion. I always thought about the Fc regions is mainly impacting NK cells. Is there something that I'm missing there or something you can help educate me on in regards to T cells and Fc receptors?

Anat Cohen-Dayag -- President and Chief Executive Officer

Sure, yes, thank you, Reni. I'll relate to the business front and then Eran can take the Fc, NK relationship. So first, COM902 was developed at Compugen in order to ensure that we extract the full potential of COM701. So we're still on this path and we want to make sure that we remain competitive on this front and that we remain flexible owning the two arms of this DNAM axis. And as you know, we just started recently the COM701, COM902 study. Having said that we're obviously open to discuss collaborative arrangements. This should allow us to continue extract the potential of COM701 and to generate some differentiation for our pipeline. So we're open to discuss collaborative arrangements spending, it will allow us to keep what we need for our own pipeline.

Reni Benjamin -- JMP Securities -- Analyst

Got it.

Eran Ophir -- Vice President, Research and Drug Discovery

About the -- and then just -- yes. So, but the role of Fc, so there are few assumptions to why preclinically people think the TIGIT is superior when it have the Fc binding. I would say maybe the leading one indeed relates in a way to enhancing NK activity, so when you use the antibody which have capability to bind Fc receptors, you enhance few mechanism that enhance, at the end of the day, depletion of the cells which carry the target TIGIT in this case.

NK activation is a major one, especially in mice. By the way, in human tumor microenvironment, you can see less NK than in mice, but also other mechanisms and people again some claim that you can get the depletion of TIGIT positive cells and since TIGIT has high expression on regulatory T cells, this is desirable, however, TIGIT has also high and overlapping expression on the CD8 T cells, the same cells you want to unleash from the TIGIT inhibitory effects and if you're going to deplete anything, you have carried the risk also of depleting CD8 T-cells in addition to Tregs and that's why we and others chose to focus on our non-Fc binders to avoid the risk of depletion of effector CD8 T cells due to enhancement of NK activity or other mechanisms of T cell depletion inside tumor microenvironment. Does this answer your question?

Reni Benjamin -- JMP Securities -- Analyst

Yes. That does. Thanks for the clarification. I guess just as a follow-up with 902, we're expecting the data from the monotherapy in the fourth quarter and you've already started the combination study, which -- what is the recommended dose for 902 or have you started at kind of the low end of the range when combining with 701 and/or escalating?

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Yes, Reni, thank you very much for your question. Yes, we did start at the low end of the range for COM902 during dose escalation. The disclosure will identify what the recommended dose for expansion for COM902 will be.

Reni Benjamin -- JMP Securities -- Analyst

Sorry, Henry, I just want to make sure. So in the fourth quarter, we'll know what the recommended...

Henry Adewoye -- Senior Vice President and Chief Medical Officer

That's correct.

Reni Benjamin -- JMP Securities -- Analyst

Got you.

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Yes, so the disclosure in the fourth quarter that Anat mentioned in her prepared remarks.

Reni Benjamin -- JMP Securities -- Analyst

Got it. Okay, thank you very much for taking the questions.

Operator

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

Asthika Goonewardene -- Truist Securities -- Analyst

Hi guys. Thanks for taking my questions. So Anat, you mentioned about the cut-offs that you think PVRL2 and PVRIG expression as selection criteria to some of the expansion cohorts. Can you tell us what was the level of expression you are looking for inclusion? And can you maybe just clarify for me please which studies you're going to be applying this inclusion criteria?

Eran Ophir -- Vice President, Research and Drug Discovery

So we are still studying it. We're following samples, we are following patients' correlation to response and this is exactly the goal of what we are trying to do to define in this stage retrospectively, which is the expression level cut-off, which could be percentage of PVRIG in the tumor microenvironment, it could be PVLR2 on the tumor cells on MIALU cells, I mean as other -- shown for other [Indecipherable]. So we're looking at all of it correlating to response and of course, looking for the right cut-off. So this is yet to be defined and it is will be defined based on data and correlations.

Asthika Goonewardene -- Truist Securities -- Analyst

Got it. And then also, I think at our last call, you mentioned -- you might have mentioned that you might be looking to present some more of the biomarker data perhaps at a conference later in 2021. Are you still on track for that or is this something we should expect more in 2022?

Eran Ophir -- Vice President, Research and Drug Discovery

We didn't disclose when exactly we'll present the data. I can only comment that we are actively and aggressively pursuing sample acquisition and correlation and then we'll present the data in the future. Ideally, we'd like to present it in scientific conferences, we still didn't disclose when.

Asthika Goonewardene -- Truist Securities -- Analyst

All right. Okay. And then maybe just to tag on to Reni's question about Bristol, but maybe approaching the other angle, so given that with -- given that Bristol may have acquired an asset that could have maybe some activity on PCRIG through the Agenus bispecific antibody deal, just want to get an idea of how involved and committed they are to doing the kind of data exploration with you or is it something that you are controlling?

Anat Cohen-Dayag -- President and Chief Executive Officer

So few things, indeed this licensing involve the TIGIT bispecific, the identity of the second arm is not known and it could be various other target. And so just to make sure that it is recognized as a product opportunity, a separate product opportunity than TIGIT. Having said that, I think it is pointing to the interest -- increased interest of BMS in the TIGIT space and that's the only thing that has shown on the behalf of BMS because obviously that's their decision-making and priority.

I will tell you that and you know it's affecting the public domain, BMS is doing studies with their own TIGIT that is part of our studies as well, but they are having studies conducted on their own with their own TIGIT. And they are committed to the collaboration with say, we're sponsoring obviously the study, the triplet study and pushing forward and that's critical for us because it's -- COM701 is the leading program in our pipeline and we want to push it forward and to have the leadership on the execution. But at the end of the day, there is investments on this program, on the TIGIT and no competition with the bispecific.

Asthika Goonewardene -- Truist Securities -- Analyst

Got it. Thanks for taking my question guys.

Operator

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

Daina Graybosch -- SVB Leerink -- Analyst

Hi, a couple of questions from me. First, on the triplet, I wonder if you can clarify what cohort you're starting to enroll in the expansion. I think initially you had plan to enroll a tumor agnostic based on PVRL2 expression with Eran's comments just now, I wonder if you wouldn't to be ready to start to enroll that patient set yet. And so could you just clarify exactly which one do you start to enroll and you'll bring on other cohorts over time? And then with that how much is BMS involved in making these clinical development strategic decisions?

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Yes. Daina, thank you very much for your question. So for the second part of the question, I'll defer to Anat to answer. For the first part of the question, as you recall for the expansion cohort, we have cohorts of patients with ovarian cancer. So that includes patients with fallopian tube cancer, that includes patients with primary peritoneal cancer and patients with epithelial ovarian cancer. The other cohort of patients in the expansion cohorts are patients with relapsed endometrial cancer. So those cohorts open through enrollment and those are the ones that we're currently exploring right now.

Anat Cohen-Dayag -- President and Chief Executive Officer

And Daina for your question about decision making, we're making joint decisions with Bristol-Myers Squibb. Obviously, we are leading this program, we're looking at every bit and piece in the -- in this program, but we are making decisions in good collaboration with the Bristol-Myers Squibb. We have very good relationship, we keep an open line of communication and we're making decisions that are good for the program together. So this is how this collaboration is being conducted.

Daina Graybosch -- SVB Leerink -- Analyst

And then so I understand that you have ovarian and endometrial open. If I recall correctly, you had planned other cohorts in the expansion, are those follow or is this reflecting some strategic change as you've seen the dose escalation data?

Anat Cohen-Dayag -- President and Chief Executive Officer

No, no, there is no strategic change -- sorry. Henry, do you want to take it?

Henry Adewoye -- Senior Vice President and Chief Medical Officer

No, go ahead and I can clarify if any.

Anat Cohen-Dayag -- President and Chief Executive Officer

Okay. No, there is no strategic change. As we stated on -- as Henry said, in the ovarian, we decided that due to the low response rate and the days total data that we have, we can continue to relate to historical data, and we'll not do the randomization. We will add the head and neck as an inflamed tumor type to this and we'll continue with the endometrial that was planned in advance. So these are three changes with respect to the basket arm that we planned to do. This is still in planning what we were saying is that we are continuing to collect data that will correlate -- continue to correlate the PVRIG pathway with the treatment response and when we will have the data that can allow us to define the cut-off for enrollment, we will start this bucket arm. So there is no change in plans on this front.

Daina Graybosch -- SVB Leerink -- Analyst

Perfect. That's very helpful. Thank you.

Anat Cohen-Dayag -- President and Chief Executive Officer

Okay.

Daina Graybosch -- SVB Leerink -- Analyst

And then on -- and then one more from me on TIGIT. I think that you guys starting back in 2009 have had your hands on a lot of different TIGIT antibody. I think you had a whole panel in your initial paper and of course, you work with the BMS, TIGIT as well as COM902. And you note the potential differentiating element of COM902 is a very high affinity. As you work up all these different TIGIT antibody, have you noted any other potential differentiating element? And I guess again asking the question, I wonder as we see your dose escalation data, you'll be the first Fc-silent TIGIT, and if you expect anything pre-clinically to show up clinically and what might we look for as we see this data in the second half or in fourth quarter?

Eran Ophir -- Vice President, Research and Drug Discovery

So yes, we did the comparison of COM902 compared to most of the leading TIGIT antibodies. What we saw that indeed COM902 has a higher affinity, higher binding to effector T cells and has good or better activity in actual functional assay. So I don't believe we saw any major differences between the other antibodies. But just COM902 is a bit superior in that -- in this regard. I would say that is difficult to say at this stage, if any of this will translate to clinical observations. Yes, potentially in terms of dosing and PK, in terms of efficacy, it'll be difficult to say if there is any -- going to be any different from the other TIGIT assets that we've seen until now.

Daina Graybosch -- SVB Leerink -- Analyst

Okay. Thank you.

Operator

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

Stephen Willey -- Stifel -- Analyst

Yes, good morning. Thanks for taking the questions. Maybe just to follow up on the Bristol collaborative question, so is your ability to I guess pursuing a triplet regimen, whether it's I guess either with or without nivo using your TIGIT COM902, is that somehow constrained by the existing Bristol collaboration? I'm just kind of curious if you see an interesting signal emerging out of the triplet, how quickly can you start to think about swapping in 902 for the Bristol TIGIT?

Anat Cohen-Dayag -- President and Chief Executive Officer

So COM902 is totally unrelated to the Bristol collaboration. This is an independent asset. Discussing the triplet, it's a little bit more complicated because the -- under the collaboration that we have with Bristol-Myers Squibb, there is an exclusivity for COM701 plus PD-1 inhibitors for a fixed period of time. So we will need to take this thing to consideration, but COM902 is totally unrelated to the collaboration with Bristol-Myers Squibb.

Stephen Willey -- Stifel -- Analyst

Okay. So I guess your ability to pursue a triplet, that would include COM701, COM902 and a PD-1 inhibitor with -- overlap with the fact that you have exclusivity to nivo tethered to COM701, is that the correct way of...

Anat Cohen-Dayag -- President and Chief Executive Officer

There are some ways for us to do it with marketed PD-1 inhibitors. So that could be done.

Stephen Willey -- Stifel -- Analyst

Okay. And then I guess you've talked on the biomarker side about doing this I guess retrospective look, whether it's a function of evaluating PVRIG expression in the tumor microenvironment and/or PVRL2, I guess on various immune cell subsets. I know that Roche had kind of previously commented that I think in their -- in one of their TIGIT presentations that they didn't believe that PVR, which is the -- I guess one of the TIGIT ligands, wasn't a great surrogate biomarker in the sense that it's kind of broadly expressed on a variety of different cell types. Is PVRL2 akin to PVR in the sense that it has that same broad pattern of expression?

Eran Ophir -- Vice President, Research and Drug Discovery

So PVR and PVRL2 in a way have similar pattern of expression in terms they do have expression also normal tissues. But both of them are upregulated in tumor microenvironment and are not -- in some tumor, you can find higher PVRL2 and some higher PVR. I think that for PVR, there [Phonetic] are also some publication may be due to its role also in enhancing other mechanisms for tumor invasive, etc. It was published also in addition to Genentech data in relation to other trials but specifically TIGIT that it correlates with worse prognosis. So yes, what Genentech have shown for PVR that in non-small cell lung cancer, it didn't seem to have correlation since it is a biomarker, it doesn't suggest a lot about PVRL2. And we'll need to -- and we are evaluating it ourselves. So we don't know. But we're to think why PVRL2 will be different than PVR.

Stephen Willey -- Stifel -- Analyst

Okay, that's very helpful. Thanks for taking the questions.

Operator

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

Tony Butler -- ROTH Capital -- Analyst

Thanks very much. Three brief questions, and let me just state them because they all relate to one another. In ClinTrials.GOV on the triple, you've made some comments today regarding the basket cohort or that of cohort three, so am I to understand that, yet the notion of what defines high expression PVRL2 is not yet known? That's question one. And if it is any color would be great?

Number two is, does PVRL2 high correlate with PD-L1 being positive or negative? And I guess a similar question may be. Are there tumors that are actually negative with respect to both markers? And then thirdly and this goes back to the SITC presentation which was quite helpful. But is there -- and this is a question that I think I hear a lot and it's never clear to me if there is a true correlation, but do peripheral effector memory CD8s and even NK-Ts, are they actually able to be found in the periphery equal to that of which is found intratumorally? That is to say, is there a direct correlation such that you don't really need the biopsy or may not need it in the future? Thank you very much.

Eran Ophir -- Vice President, Research and Drug Discovery

So for the first question, so what is high PVRL2? So this is exactly what we're looking at, to define what is the cut-off, score of 100 or 200 or percentage of immune cells expressing PVRL2 or other DNAM axis members, what is the cut-off that determines and correlates best with response? So this will be determined retrospectively and then tested clinically prospectively. This is for the question of the what is high PVLR2.

About PVLR2 versus PD-L1, so this is a very important question and PVRL2 in contrast to PD-L1 is not induced by inflammation. And therefore, you can find high PVRL2 in PD-L1 positive but also in PD-L1 negative tumor types. And that's why we pre-identified, for example, ovarian and endometrial and other tumor types which sits in some of them the expression of PD-L1 is not very high. The response to PD-1 is not very high, but PVLR2 and in general, the PVRIG pathway is very dominant there and that's why we're trying to attack these kinds of tumor types.

About the effector memory and NK-T, so the correlation between effector memory cells proliferating in periphery and specific effector clones proliferating inside tumor macroenvironment exits. I wouldn't say that we and the entire scientific community is in a place that we can rely solely on the peripheral measurements and that's why we have third biopsies in the expansion course of our trials to look inside tumor microenvironment but there is a correlation and in many cases, you see specific clones that are proliferating peripherally and they're also expanding inside tumor microenvironment.

NK-T, you can find a bit less of those in tumor microenvironment but there are studies to show that during they are present, they are correlated to mostly to good prognosis, the correlation between peripheral and intratumoral expansion of NK-T, I wouldn't believe it was investigated much or it is, I'm not aware of any studies to correlate that, but just to mention, in addition to what it reflects about the tumor microenvironment, this kind of intense proliferation also supports that the drug COM701 is active and it does -- again this is preliminary data. But what it suggests that it does, what you think it should do, enhance immune cells activity, enhance interferon gamma. So this is another surrogate marker for drug activity in addition to the direct correlation to what is happening in tumor microenvironment.

And maybe just to add that this is may be in many cases also for other drugs when you, especially in early trials has heavily pre-treated patients, you can find this kind of pharmacodynamic changes in the tumor, in the periphery. And they're not always correlated to response.

Tony Butler -- ROTH Capital -- Analyst

Thank you. One follow-up if I may though, this is back to the second part of PVRL2 and PD-L1, but if you were able, post-therapy, if in fact you actually drive PD-L1 expression, even in PD-L1 minus tumors, when you look at a tumor initially having been treated with something else that is in fact relapse or a relapsed patient or a resistant patient, a PD-L1 minus patient and in fact then treated with COM701, for example, would drive PD-L1 expression. Is that true?

Eran Ophir -- Vice President, Research and Drug Discovery

If indeed and as mentioned before, the biology of PVRIG and PVRL2, if we will be able to drive and expand this in tumor microenvironment then potentially, we'll increase the inflammatory status of tumor macroenvironment and then potentially PD-L1 could be upregulated as well as a marker to indicate and again this is one of the reasons PD-L1 is a biomarker for PD-L1 activity while it reflects [Indecipherable] is more inflamed and has more T cells inside.

Tony Butler -- ROTH Capital -- Analyst

Exactly. And thank you very much.

Operator

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?

Anat Cohen-Dayag -- President and Chief Executive Officer

Thank you. To conclude, we're excited about what's to come and are proud of our remarkable progress. As always, we will seek to continue to drive the science to uncover important insights into the biology and mechanism of our candidate and we remain uniquely positioned to unlock the promise of these potentially foundational immunotherapy candidates in the clinic across patient population typically considered unresponsive to current treatment. Thank you for joining us today and your continued support. Stay safe and healthy.

Operator

[Operator Closing Remarks]

Duration: 58 minutes

Call participants:

Yvonne Naughton -- Head of Investor Relations and Corporate Communications

Anat Cohen-Dayag -- President and Chief Executive Officer

Ari Krashin -- Chief Financial and Operating Officer

Eran Ophir -- Vice President, Research and Drug Discovery

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Mark Breidenbach -- Oppenheimer & Co., Inc. -- Analyst

Chris Howerton -- Jefferies LLC -- Analyst

Reni Benjamin -- JMP Securities -- Analyst

Asthika Goonewardene -- Truist Securities -- Analyst

Daina Graybosch -- SVB Leerink -- Analyst

Stephen Willey -- Stifel -- Analyst

Tony Butler -- ROTH Capital -- Analyst

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