Compugen Ltd (CGEN) Q3 2021 Earnings Call Transcript

Image source: The Motley Fool.

Compugen Ltd (CGEN 0.52%)
Q3 2021 Earnings Call
Nov 12, 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's Third Quarter 2021 Results Conference Call.

[Operator Instructions]

I would now like to introduce Yvonne Naughton, Head of Investor Relations and Corporate Communications. Yvonne, please go ahead.

Yvonne Naughton -- Head of Investor Relations and Corporate Communications

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 prepared remarks are Anat Cohen-Dayag, President and CEO; Henry Adewoye, CMO and Ari Krashin, Chief Financial and Operating Officer. For the Q&A session, we will also be joined by and Eran Ophir, Vice President, Research and Drug Discovery.

Moving to Slide 2. Before we begin, I would like to remind you, that during this call, the company may make projections that are forward-looking statements regarding future events or business outlook, our development efforts and their outcome, 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 should caution you that such statements reflect only on the company's current beliefs, expectations and assumptions, while actual results, performance or achievements of the company may differ materially. These statements are subject to the 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 annual report on Form 20-F filed on February 25, 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

Slide 3 please. 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 three presentation at SITC, providing clinical, translational and preclinical data that demonstrates strong execution across our differentiated clinical and scientific strategy and to further support to our path forward. Indeed, to our knowledge, this is the first data presentation ever of a triple blockade of PVRIG TIGIT and PD-1 and the first time data on anti-tumor activity of an Fc reduced effector function anti-TIGIT antibody is presented in a scientific conference. These dose escalation studies cleared our path to initiate multiple expansion cohort studies that are designed to grow the evaluated inhibition of the DNAM axis in cancer immunotherapy and advance the therapeutic development of our two 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 four 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 immune-oncology research with the ultimate goal of developing new therapies. We have an impressive track record of driving the discovery of new targets and pathways in the immune-oncology space with cutting-edge science published in peer-reviewed paper and development of a clinical stage pipeline derived from this science. Our clinically validated computational target discovery platform has generated a pipeline of exciting new candidates that are being evaluated in Phase 1 clinical trial by us and our partners, including our potentially first-in-class anti-PVRIG antibody COM701, our high affinity IgG4 Fc reduced effector function, anti-TIGIT antibody COM902, bapotulimab, an anti-ILDR2 antibody which is being developed by Bayer and AstraZeneca's TIGIT bispecific antibody program derived from COM902. I'm proud of our talented team of scientists with expertise in immuno-oncology and translational medicine and with our capabilities of driving the signs of new unexplored biological pathway forward as we develop first-in-class therapeutics targeting this pathway.

This takes us to our second pillar, which is to expand the number of patients responding to treatment by developing potentially first-in-class therapies for patients non-responsive or refractory to currently available therapies. Specifically, the unique biology we unlocked for the PVRIG pathway following its discovery served as the basis for our assessment of the different combinations of PVRIG, TIGIT and PD-1 inhibitor in select biomarker informed tumor types, generally not responsive to checkpoint inhibitor. What makes us differentiated beyond the discovery of this pathway and uncovering the potential role within the DNAM axis is that we are the only company evaluating combination of PVRIG, TIGIT and PD-1 blockers in the clinic. It is exciting to be the leaders in the DNAM axis, especially considering the recent advancements and raising interest by followers in this area.

Maximizing the value for patients is our third pillar, and speaks to our goal of bringing new treatments to market as rapidly and efficiently as possible. To support us on our journey, we seek collaborations and strategic partnerships with leading biopharma companies with complementary capabilities worldwide to expedite our early and clinical stage programs, and bring them to the market. In addition to our partnership with BMS, our partnerships with AstraZeneca and Bayer also highlight the value of our strategy to broaden the opportunity for products to reach more patients.

And finally, our fourth pillar is to protect our innovation while developing drugs for patients through securing IP rights. We have developed a strong IP portfolio with potentially broad protection for drug candidates.

Now moving to Slide 5. We've employed a comprehensive clinical strategy to assess our DNAM axis hypotheses. We designed multiple combination studies evaluating the simultaneous blockade of the three pathways and subset all are running now in parallel in multiple tumor types selected in a biomarker informed manner. Each of these studies include comprehensive translational data analytics in order to further support our drugs mechanism of action, and discover and evaluate potential biomarkers that may be of relevance for future patient selection. In addition, our multiple combination studies are being pursued in some overlapping indications. This is by itself, will allow us to evaluate the contribution of each drug in these combinations. And focusing mainly on non-responsive tumors should help to differentiate the contribution of COM701.

The data from these multiple studies will allow us to select the combinations and tumor types to progress our program. Moving now to slide 6. Delighted to say that we delivered on all our targeted milestones for this quarter and for the year. 2021 played a major role in further solidifying our leadership position in the DNAM access, with steady and impressive execution. We've completed all our dose escalation studies, including our COM701 monotherapy, COM701 plus nivolumab, COM902 monotherapy, and triple combination studies. We've now progressed to expansion cohort across all our programs, which allows us to focus on select indications to our translational data-driven approach.

Our accomplishments through 2021 also reinforce the power of our partnering strategy in diversifying our portfolio with a milestone payment from AstraZeneca after the first patient dose in their Phase 1 study of TIGIT bispecific, derived from our COM902. In addition, we were thrilled to announce the expansion of our collaboration with BMS. and believe the recent $20 million strategic equity investment in Compugen strengthens our relationship and the goal of both companies to bring innovative therapies to cancer patients through the advancement of our clinical studies conducted under our collaboration.

As part of the expansion of the collaboration, a joint steering committee has been formed to facilitate strategic oversight and guidance for the programs run under the collaboration. This committee will run alongside the existing joint development committee, which acts at an operational level. With that I'd like to turn the call over to Henry for him to provide an overview of our data released at SITC today, Henry.

Henry Adewoye -- Senior Vice President and Chief Medical Officer

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' 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 are enrolling patients with platinum resistant ovarian cancer, endometrial cancer, and head and neck squamous cell cancer. We also reported on preliminary anti-tumor activity and reported stable disease in three patients with one 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 TNN T-cell [Phonetic] activation and memory T-cell proliferation at all doses of COM701. These results are significant for several reasons. They are consistent across measures and patients. And the magnitude of the effect was above what has been observed in monotherapy and well-combination settings of COM701 blockade, as well as published results for other TIGIT antibodies, mono and combination studies. They support a potent activation of the immune system, following triple blockade of PVRIG, TIGIT and PD-1, and aligns with an extensive preclinical work predicting this effect. It is also important to highlight that immune activation was achieved in our studies in historically cold tumor types, including ovarian, colorectal, and prostate cancer.

Together, these results further support Compugen's earlier finding for the potential of triple blockade to drive synergistic immune activation, and we look forward to the continued evaluation of our hypothesis in the ongoing biomarker informed expansion cohorts. In staying with the theme of translational data, I will take a minute here to mention some of the preliminary findings that will be presented here at SITC in our research booster. Following up on our observation, the PVRIG is a potential unique and dominant checkpoint involved in stem-like memory T-cell dendritic cell interaction. We evaluated serum from the two patients who responded to a combination of COM701 and nivolumab.

Interestingly, we saw an increase in markers of dendritic cell activation in these patients when compared to non-responding patients. This may suggest that this clinical response involved enhanced dendritic cell T-cell interaction triggered by COM701. It is exciting to see that our research relating to PVRIG potential mechanism of action translates to preliminary findings in the clinic, and further supports the differentiation of PVRIG from TIGIT and PD-1. This also suggests a differentiated profile for COM701 having a potential to address both inflamed and less inflamed tumor types where current checkpoint inhibitors have not been successful, and further explains why one might expect a more potent immune activation when combining COM701 with the other inhibitors.

Moving next to Slide 9 and to the SITC data from our Phase 1 dose escalation study, evaluating high affinity anti-TIGIT antibody COM902 with reduced Fc effector function. The study enrolled 18 patients with advanced solid tumors, that is, all comers, who exhausted all available standard therapies and were heavily pre-treated with a median of seven prior therapies and maximum of 16. The primary objectives of this COM902 monotherapy dose escalation study was to establish safety and tolerability, the recommended dose for expansion and the PK profile of COM902. Overall, COM902 demonstrated a favorable safety and tolerability profile.

In the study, we reported two patients with dose-limiting toxicities, one patient in the single subject dose cohort with Grade 2 vomiting at 0.01 milligram per kilogram dose, and one patient with Grade 3 atrial fibrillation at the 1 milligram per kilogram dose. These DLTs were based on assessment by the investigator. It is important to note that there were no DLTs reported at any other doses, including the higher doses up to 10 milligram per kilogram, and a maximum tolerated dose was not reached. Of note, in the COM902 repeat those pre-clinical study, no ECG changes were noted. The COM902 3 milligrams per kilogram IV Q3 week was selected as the recommended dose for expansion. Additionally, the PK of COM902 was dose proportional and support Q3 week dosing.

We were encouraged by preliminary anti-tumor activity with 50% of patients or nine of 18 achieving a best response of stable disease with six patients, 67% with confirmed stable disease and three patients, 17% with stable disease of at least six months duration or longer. And while we consider TIGIT to be a combination therapy, achieving a disease control rate of 50% in this heavily pre-treated patient population is encouraging. These preliminary results are particularly significant for Compugen and the broader TIGIT space.

As you may know, there is an ongoing debate regarding the role of the Fc domain and its relevance for anti-tumor activity with TIGIT inhibitors. Our approach has always been to have reduced Fc effector function anti-TIGIT antibody, as we believe, this reduces the risk of depleting CD8 positive T-cells, which are crucial for driving anti-tumor activity. These signals of preliminary anti-tumor activity with COM902 mono-therapy are suggesting that are reduced Fc approach is an appropriate strategy, and this is supported by the translational data, which I show on the next slide. Now, moving to my last slide, slide 10, we see translational data from the study that further explore this.

Through cytometry analysis of peripheral blood from patients treated with COM902 shows no significant changes in TIGIT positive CD4 and CD8 T-cells and NK cells. This is important as this result reinforce that our reduced Fc approach avoid the depletion of major TIGIT positive lymphocytes, which are critical for anti-tumor immunity, and as I indicated earlier, support our rationale for choosing an IgG4 Fc reduced effector function anti-TIGIT antibody. Before I turn the call over to Anat, I'd like to thank the patients and their families, investigators, and study sites. Anat.

Anat Cohen-Dayag -- President and Chief Executive Officer

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 blockade, which is consistent across tumor 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 two patients has clinically responded to COM701 plus nivolumab treatment. This new preliminary observation suggest that a unique dendritic cell 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 TIGIT front, our ultimate strategy is in combination settings and our position is unique in evaluating PVRIG and TIGIT dual blockade in the clinic with our ongoing COM701, COM902 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 COM902 avoids depletion of major TIGIT positive lymphocytes, including CD4 and CD8 T-cells, as well as NK cells, while 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 three 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 has enabled our remarkable accomplishment. I'll now turn the call over to Ari to review our financials. Ari.

Ari Krashin -- Chief Financial and Operating Officer

Thank you, Anat. So, moving to Slide 12. Our financial results for the third quarter of 2021 released this morning continued 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 30, 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 $113 million to $116 million. The company has no debt.

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

Questions and Answers:

Operator

Thank you. Ladies and gentlemen, at this time, we will begin the question-and-answer session.

[Operator Instructions]

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

Mark Breidenbach -- Oppenheimer -- Analyst

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 mg/kg 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.

Anat Cohen-Dayag -- President and Chief Executive Officer

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

Henry Adewoye -- Senior Vice President and Chief Medical Officer

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 Q3 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 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 their dose, it's very similar across companies. So, we're not -- we're actually in the mainstream.

Eran Ophir -- Vice President, Research and Drug Discovery

Maybe just to add, and 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 this translated also into achieving full RO, receptor 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 -- will be sufficient to allow for full-year occupancy also in the tumor micro-environment.

Mark Breidenbach -- Oppenheimer -- Analyst

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?

Henry Adewoye -- Senior Vice President and Chief Medical Officer

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 three patients or two patients, and the single-digit toxicities might 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.

Mark Breidenbach -- Oppenheimer -- Analyst

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

Operator

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

Stephen Willey -- Stifel -- Analyst

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 function?

Eran Ophir -- Vice President, Research and Drug Discovery

Yes. So, some of the companies did publish these results. And what they have shown is dramatic reduction. It 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 in tumor microenvironment. When peripheral blood, they have shown depletion of CD8 positive TIGIT positive cells in the peripheral blood and the reduction was dramatic.

Stephen Willey -- Stifel -- Analyst

Okay, that's helpful. And then on the triple combo biomarker data that you have again, I guess it appears to kind of 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?

Eran Ophir -- Vice President, Research and Drug Discovery

Okay. So, in this trial in the triplet study, the dose response range was not as big as we had in the past, so actually we started in one patient in all three and then already moved to 1 mg/kg which is already for receptor occupancy. So, in this specific context, we haven't seen much of a dose response. And remind that in the past we had a wider range of responses, concentrations we did see a dose response of COM701 in combination with nivo etc.

Stephen Willey -- Stifel -- Analyst

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 stay in your own way.

Anat Cohen-Dayag -- President and Chief Executive Officer

I'll relate to that, Steve. So, this collaboration -- actually this expansion of the collaboration reflects on the long-term -- long-standing relationship between the two 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 strategy 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 COM701 [Phonetic] nivolumab 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, that 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. So 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.

Stephen Willey -- Stifel -- Analyst

All right. Thanks for taking my questions.

Operator

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

Daina Graybosch -- SVB -- Analyst

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? There's not so much shrinkage and a lot of stable. Any notable case studies that gave you a lot of confidence.

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Thank you very much for the question, Daina. So 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 swimmer plots. We think that the swimmer plot best represents how heavily pre-treated those patients were. We also provided icons in the swimmer plot 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 swimmer plot. 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.

Daina Graybosch -- SVB -- Analyst

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

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Yeah, we decided not to include that because -- since it was not an eligibility criterion, 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 swimmer plot. So if you see the -- on that swimmer plot, we have of the 18 patients, nine of them with either best response assessment of stable disease, and out of this nine, two-third, 67% with confirmed stable disease. And of course, three patients with stable disease that's six months or longer. The icons that we illustrate in the swimmer plot I think provides a surrogate assessment for how COM902 as mono-therapy through those escalation 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.

Daina Graybosch -- SVB -- Analyst

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

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Yes. We had certain benchmarks in the protocol with regards to eligibility for enrollment onto the study. So of all the patients that we had, out of those 18 patients we enrolled, eight of them had received prior immune checkpoints. And we -- if you look at the swimmer plot, it best illustrates those patients that I can just go through them. So, we had a patient with a chordoma [Indecipherable] carcinoma, peritoneal cancer, small cell lung cancer, [Indecipherable] prostate cancer, renal cell carcinoma and prostate cancer. Yes, we follow the guidelines in terms of wash out.

Daina Graybosch -- SVB -- Analyst

Perfect. Okay. Thank you very much.

Henry Adewoye -- Senior Vice President and Chief Medical Officer

No worries.

Operator

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

Chris Howerton -- Jefferies -- Analyst

Hi. Good morning. 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 two 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.

Henry Adewoye -- Senior Vice President and Chief Medical Officer

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 these questions and do the lab work on the patients, reported or observed is also. We think that based on the mechanism of action of COM902, and also as part of the trip let, that the toxicities that we've observed, are toxicities that are not unique, highlight to COM902, or the toxicities that are unique as part of the triplet. 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 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.

Chris Howerton -- Jefferies -- Analyst

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

Operator

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

Tony Butler -- ROTH Capital -- Analyst

Yes, thanks very much. The question or series of questions. One is on, in the triple study, a small number of patients, but what is considered a high expresser of PVRL2, that's question one. And then question two, 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, and I realize that the translational data is all peripheral, we don't really know what goes 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.

Eran Ophir -- Vice President, Research and Drug Discovery

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 this indication which PVRL2 in terms of age score, if you wish, it's probably 200, 300 and so this is 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.

Henry Adewoye -- Senior Vice President and Chief Medical Officer

You're correct that the duration is a reflection of the heavy pre-treatments that the patients 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 a median of ten prior therapies with a range of one through 19, and if you think of the COM701 nivo study, this was a median of five. So, it's actually essentially a doubling of the median type therapies. So 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.

Eran Ophir -- Vice President, Research and Drug Discovery

And then for the third one. So about 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 three 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 immune activation reflected by the potency, by the consistency, and evident by multiple read-outs 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 and combination, and also to all published data that we're aware of, of TIGIT and mono and combinations, the effects still seems again more and more robust and more potent, again suggesting that the triplets is 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 in tumor microenvironment in order to actually see tumor shrinkage. So, while we are following biopsies and want to expand the trial and also look at new microenvironment, these 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 course.

Tony Butler -- ROTH Capital -- Analyst

Excellent I am grateful. Thank you very much.

Operator

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

Reni Benjamin -- JMP Securities -- Analyst

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.

Henry Adewoye -- Senior Vice President and Chief Medical Officer

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 part of the expansion for the triplet.

Reni Benjamin -- JMP Securities -- Analyst

Okay. And then as you guys have looked at this data, have 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 or you might be able to use in your expansion cohorts?

Eran Ophir -- Vice President, Research and Drug Discovery

So, I would say that again, the main observation is just mentioned the translational data in peripheral 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, we will explore also modulation in the tumor microenvironment. But this is all work in progress.

Anat Cohen-Dayag -- President and Chief Executive Officer

Reni, I just --

Reni Benjamin -- JMP Securities -- Analyst

Sorry. Go ahead, Anat.

Anat Cohen-Dayag -- President and Chief Executive Officer

I just -- I was just going to say that in general, and Eran was alluding to it, the fact that we were observing potent immune activation in the triplet, in the doublet, 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 DNAM axis hypothesis. So at this point in time, this is what we have, but we are encouraged with this.

Reni Benjamin -- JMP Securities -- Analyst

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 study? Ad 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.

Anat Cohen-Dayag -- President and Chief Executive Officer

So I'll start answering this and Henry if you have any additional feel free to chime in. 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 /PDL-1 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.

Henry Adewoye -- Senior Vice President and Chief Medical Officer

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/ PDL-1 axis, but also to rely on the strength that Compugen has with its antibodies. So we also think strategically of a PD-1 and the PDL-1 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, PDL-1 combination, but one that is free of those agents.

Reni Benjamin -- JMP Securities -- Analyst

Great, thanks for taking the questions.

Operator

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

Asthika Goonewardene -- Truist Securities -- Analyst

Hey guys. Thanks for taking my questions. Apologies if any background noise, I am at the Floyd city here. 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 to us a little bit about what were the signals that you might have been seeing that sort of been driving the progression after the therapy. Thanks.

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Yeah, Asthika that's a good question. So, for patients, because it's data that we're presenting, is that dose escalation. Biopsies are not mandatory, as opposed to patients who are 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 biopsies on any of these subjects or one subject to the other ongoing or the subjects who had stable disease or the subjects who progressed.

Asthika Goonewardene -- Truist Securities -- Analyst

Great. Thanks for taking my question, guys.

Operator

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?

Anat Cohen-Dayag -- President and Chief Executive Officer

Yes. Thank you, Operator. Thank you for joining us today and your continued support. We hope to see you here at SITC. Stay safe and healthy.

Operator

[Operator Closing Remarks]

Duration: 62 minutes

Call participants:

Yvonne Naughton -- Head of Investor Relations and Corporate Communications

Anat Cohen-Dayag -- President and Chief Executive Officer

Henry Adewoye -- Senior Vice President and Chief Medical Officer

Ari Krashin -- Chief Financial and Operating Officer

Eran Ophir -- Vice President, Research and Drug Discovery

Mark Breidenbach -- Oppenheimer -- Analyst

Stephen Willey -- Stifel -- Analyst

Daina Graybosch -- SVB -- Analyst

Chris Howerton -- Jefferies -- Analyst

Tony Butler -- ROTH Capital -- Analyst

Reni Benjamin -- JMP Securities -- Analyst

Asthika Goonewardene -- Truist Securities -- Analyst

More CGEN analysis

All earnings call transcripts