Iteos Therapeutics Inc

NASDAQ:ITOS

Earnings Call Transcript 2021-Q1

[Operator]

Good afternoon and welcome to the iTeos Therapeutics First Quarter 2021 Financial Results Conference Call. At this time, all participants are in a listen-only mode. Following the formal remarks, we will open the call up for your questions. Please be advised that this call is being recorded at the company's request.

Now I'd like to turn over to Ryan Baker, Head of Investor Relations at iTeos. Sir, please proceed.

[Ryan Baker, Head of Investor Relations]

Thank you for joining us today. Joining me from iTeos are Michel Detheux, President and CEO; Dr. Joe Lager, Chief Medical Officer; and Matthew Gall, Chief Financial Officer.

Before we begin, I would like to remind you all that the team will be making forward-looking statements in the prepared remarks and during the Q&A session. Any statements made during this call that are not statements of historical or current facts are intended to be forward-looking statements pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995.

We want to emphasize that such forward-looking statements reflect our current expectations and assumptions regarding timing, progress and success of our current ongoing clinical trials, therapeutic potential thereof, planned regulatory submissions, our financial condition, our business operation, development efforts and relationships with third parties and collaborators, and are neither predictions nor guarantees of future events or performance.

Actual results could differ materially from those stated or implied by these forward-looking statements due to risks and uncertainties associated with our business, including those under the heading entitled Risk Factors in our annual report on Form 10-K for the year ended December 31, 2020, and our quarterly report on Form 10-Q for the quarter ended March 31, 2021. That will be filed with the SEC today and in subsequent reports, including our current reports on Form 8-K. Company disclaims any obligation to update or revise any forward-looking statements except as required by law. Michel?

[Michel Detheux, President and Chief Executive Officer]

Thank you very much, Ryan, for the introduction and thank you for joining us for our first quarter 2021 earnings call. For today’s call, I will provide a brief recap of our corporate strategy and overview of projects within our pipeline programs, as well as the multiple opportunities and readouts for our clinical programs. And we'll turn the call over to Dr. Joe Lager, our Chief Medical Officer to provide the status update and review of our most recent results from our ongoing clinical trials. Finally, our Chief Financial Officer, Matthew Gall, would summarize our financial status after which I’ll return for closing remarks. We will be all available for the Q&A session.

I would first like to highlight the key strength of iTeos as a cancer immunotherapy company. We are developing therapies focus on wild-type target mechanisms of immunosuppression. Our approach involves targeting pathway that reduces cancer immunosuppression of the immune system and our goal is to develop therapies with the potential to fully restore the immune response against cancer. Through the first quarter of 2021, we continue to advance our differentiated clinical programs, EOS-448, our potent high affinity anti-TIGIT antibody and inupadenant, a potent highly selective A2A receptor antagonist. We shall hope this clinical strategy to strengthen our position in the cancer immunotherapy space.

We have highly encouraging initial data and are pleased with the activity on safety profiles we have observed with single agent monotherapy. In both our clinical programs we think that the immunotherapy responses that we have seen with our programs are a series of differentiations. We are looking probably to continuing the development of these drugs in combination, where we see the most potential to benefit patients. We have combinations to these well underway with inupadenant, and we'll be initiating combination with EOS-448 this year.

With our headquarters in Cambridge, Massachusetts and our R&D center in Belgium, iTeos’s global presence allowing us to attract talent worldwide and remain at the forefront of innovation in the field of immuno-oncology.

Lastly, we are well capitalized with a runway well into 2023. The [indiscernible] flexibility to follow the data and competitive landscape in the design of our clinical plan we saw significant financial constraint. In summary, this is an exciting time for iTeos, which we continue to make progress advancing our two clinical programs and our ongoing discovery effort with the goal of improving the life of people with cancer. Our recent data presentation for our anti-TIGIT antibody with 448 at AACR showcase a favorable safety and tolerability profile, encouraging things, signs of clinical efficacy, including disease stabilization and one partial response. And physical depletion of immunosuppressive Treg and exhausted T cells in periphery in patient with advanced cancer.

While Joe will provide a more detailed review of the data and our clinical development plan later in the call, I would like to highlight that our complete data align, which is now better than other anti-TIGIT space. We are initiating Phase 1b/2 combination trails in both checkpoint naive and resistant patients. We expect that our work over the next 12 to 18 months will comes from the position of our TIGIT program within the immuno-oncology treatment landscape.

We are also advancing our second clinical program, the highly selective adenosine A2A receptor antagonist, inupadenant. At ASCO in June, we will report updated results from our monotherapy dose escalation study. In our view, the unique potential of inupadenant is bet on its high-potency and productivity for the A2A receptor. The resistant to attenuation by higher adenosine patient form in the tumor microenvironment. The favorable efficacy and safety profile is demonstrated by the Phase 1 data presented last year at ACR and identification of potential predictive biomarker based on the expression of A2A receptor in the tumor microenvironment.

We are evaluating inupadenant in combination with pembrolizumab with chemotherapy and with EOS-448 in these specific cohorts. Inupadenant with the process of our clinical programs, we are also advancing research programs, focus on target that compliment the mechanism of action of A2A receptor and TIGIT programs and address additional mechanisms of immunosuppression. We are building our pipeline and expect to nominate an additional product candidate for IND-enabling studies before the end of 2021.

So our strategy, TIGIT is an exciting new immuno-oncology target with external validation. And we have demonstrated that EOS-448 potently engage with the target under Fc gamma receptor. We are exploring new opportunities to accelerate and expand our development plans potentially through our strategic partnerships. Adenosine plays an important role in immunosuppression in the tumor microenvironment. And there have been some encouraging signals of activity with adenosine receptor, another pathway target. Our inupadenant program will design new properties to overcome the limitation of other drugs in its class. And we look forward to achieving clinical the proof of concept in the ongoing unplanned trials in the near future.

I will now pass the call over to our Chief Medical Officer, Joe Lager, to discuss the progress in clinical development of both of inupadenant and EOS-448 in more detail. Joe, please.

[Joe Lager, Chief Medical Officer]

Thank you, Michel. I'd like to begin by providing a summary and the progress with our adenosine receptor antagonist, inupadenant, for which we'll be presenting an update at ASCO next month. The adenosine pathway is a critical mechanism, which suppresses the immune response against tumors and then inhibits responses to current cancer therapies. There are multiple potential therapeutic targets in the adenosine pathway. The adenosine receptor A2AR is a key receptor responsible for mediating adenosine’s immunosuppressive effects on immune cell.

A2AR is highly expressed on effector immune cells and potent inhibition of A2AR has the potential to block immunosuppressive signaling and restore an anti-tumor immune response. We selected this critical target based on our characterization of unique conditions of the tumor microenvironment. We thought to design a therapeutic that could selectively and potently inhibit A2AR, despite the high concentrations of adenosine presence in the tumor microenvironment.

Inupadenant is a next generation A2AR antagonists with differentiated pharmacologic properties. Unlike prior generations of adenosine receptor antagonists, inupadenant was designed to inhibit A2AR even at high concentrations of adenosine. Inupadenant is also highly selective for A2AR, it has minimal blood-brain barrier penetration properties which are expected to reduce off-target safety effects and improve the therapeutic index.

We're currently evaluating inupadenant in several Phase 1b/2a studies, both as a monotherapy and in combination with pembrolizumab or chemotherapy. The results from the dose escalation portion of the Phase 1 study in patients with advanced stage cancer were presented at AACR last year. And showed that inupadenant was well-tolerated with no dose limiting toxicity. In addition inupadenant demonstrated clinical benefit as monotherapy across multiple heavily pretreated advanced cancers with durable partial responses seen in the patient with checkpoint inhibitor resistant melanoma and in the patients with heavily pretreated castrate-resistant metastatic prostate cancer.

We've also shown that when given twice daily, all of the tested doses resulted in a full inhibition of A2AR signaling at 24 hours after dosing. These results have generated much excitement for the program. And we look forward to presenting an update on our monotherapy cohort at ASCO next month which will be focused on the tumor biomarkers evaluated in this study and the finding that the expression of the A2A receptor in the tumor may be associated with clinical outcomes.

We're currently executing a multi-arm Phase 1/2a clinical trial in adult patients with advanced solid tumors, where there's a strong rationale for treatment with an A2AR antagonist. We're enrolling patients in four distinct cohorts as both a single agent and in combination approaches. We have two cohorts evaluating inupadenant in patients with castrate-resistant – castrate-resistant metastatic prostate cancer, one is monotherapy and the second cohort in combination with pembrolizumab.

The third cohort is evaluating inupadenant in combination with pembrolizumab in patients with checkpoint inhibitor resistant melanoma. The fourth cohort is evaluating inupadenant in combination with chemotherapy in patients with triple negative breast cancer. We will continue to integrate a biomarker driven approach into our A2AR clinical programs to choose optimal therapeutic combinations and identify the patients most likely to benefit from treatment.

I will now provide an overview of our process with EOS-448, our highest affinity potent anti-TIGIT antibody with a functional Fc domain, designed to enhance the anti-tumor response through a multifaceted immune modulatory mechanism. EOS-448 has the potential to achieve significant immune stimulatory effects through three mechanisms. One, blocking the binding of TIGIT to slide down, resulting in immune-mediated killing of tumor cells, two, engaging the FC gamma receptor expressing receptor cell, that further promote anti-tumor immune responses, including through the release of pro-inflammatory cytokines and chemokine and the activation of antigen presenting cells and three, depleting cells that are known to dampen the immune response, immunosuppressive Tregs and exhausted T-cells.

Last month at AACR Dr. Van den Mooter presented first in-human data from the open label dose escalation Phase 1 portion of the clinical trial in patients with advanced solid tumors. We were very pleased to report encouraging signs of clinical benefit with EOS-448 as a monotherapy in patients with advanced cancer. Of note, we observed a confirmed partial response with single agent treatment with EOS-448 in one pembrolizumab refractory BRAF mutant melanoma patient.

We also observed a non-lethal safety profile consistent with other drugs within this class and all of the tested doses were generally well-tolerated. Our peripheral biomarker data demonstrated TIGIT positive Treg depletion and a reduction in exhausted TIGIT positive CD8 T-cells, reinforcing our initial hypothesis about the FC gamma receptor engagement activity of EOS-448. These robust biomarker data coupled with the preliminary signs of efficacy as a monotherapy indicate that EOS-448 is highly active with strong on target immune responses and may potentially drive even stronger responses in combination studies.

Based on these early positive results, we're pursuing a robust clinical development time for EOS-448 with new combination approaches and three checkpoint-naive and checkpoint-resistant settings. We will assess the combination of EOS-448 with PD-1 inhibition in patients where pembrolizumab is indicated as a monotherapy, but where the addition of EOS-448 may improve clinical benefit to patients. We will first assess the safety of the combination of EOS-448 with pembrolizumab in solid tumors and then we'll move into disease specific trials in first line non-small cell lung cancer and heading next squamous cell cancer, where we'll assess both the PD-L1 high and PD-L1 low populations.

We are also planning to evaluate the combination of inupadenant and EOS-448 in patients with checkpoint inhibitor resistant melanoma and EOS-448 in combination with an IMID in relapsed or refractory multiple myeloma. We're planning to start these studies in mid-2021 and are continuing to evaluate our clinical development plans for EOS-448 in other solid tumors, including triple negative breast cancer, gastric cancer and pancreatic cancer.

I now hand the call over to Matthew Gall, our Chief Financial Officer.

[Matthew Gall, Chief Financial Officer]

Thanks, Joe. I'd like to provide a brief update on our financial results for the first quarter of 2021. The company's cash and cash equivalent position was 321.4 million as of March 31, 2021 as compared to 147.7 million as of March 31 of 2020. We project that based on our current clinical plan, this cash balance provides a runway well into 2023.

Research and development expenses were 11.6 million for the quarter ended March 31, 2021 as compared to 5.8 million for the first quarter of 2020. This increase was primarily due to an increase in activities related to clinical trials for inupadenant and EOS-448, and increased headcount. General and administrative expenses were 7 million for the quarter ended March 31, 2021 as compared to 2.4 million for the first quarter of 2020. The increase was due primarily to increased headcount and professional fees and other costs associated with becoming a publicly traded company.

The net loss attributable to common shareholders was 13.5 million or a net loss of $0.39 per basic and diluted share for the quarter ended March 31, 2021 as compared to $6.5 million or a net loss of $25.53 per basic and diluted share for the first quarter of 2020. I'll now turn the call back over to Michel for closing remarks.

[Michel Detheux, President and Chief Executive Officer]

Thank you, Matt. As outlined on this call we are continuing to make progress, advancing our two clinical programs and our ongoing discovery efforts to move forward with our mission to improve the lives of people with cancer. With the upcoming data update of inupadenant in ASCO in June, we continue to progress our clinical execution.

We are focused on our differentiated clinical development plan for both program and we anticipate that the next 12 to 18 months will be pivoted to establishing the position of EOS-448 in the TIGIT space, particularly as we evaluate EOS-448 new combination approaches in both checkpoint-naïve and checkpoint resistant settings.

We believe both inupadenant and EOS-448 have the potential to improve outcomes for cancer patients, which have all kinds of cancers. With our deep understanding of cancer immunology and the biology of immunosuppression we will continue to strengthen our pipeline for the development of cancer immunotherapy.

Thank you very much for your attention on today’s call and your ongoing interest. I’d like to now turn the call back over to the operator for questions.

[Operator]

Thank you, speakers. [Operator Instructions] First question is from Chris Raymond of Piper Sandler. Your line is now open.

[Chris Raymond, Piper Sandler]

Hey, thanks guys. Just a couple of questions on EOS-850. I guess during your AACR call, you guys noted and I think you also talked just now on this that you have data at ASCO. But I think you also framed sort of the next big update for that program would likely be a second half of that. And I guess we were thinking SITC was maybe the more appropriate venue. Can you maybe just provide some clarity, I guess, around what we should expect to see at ASCO, maybe frame that for us a little bit?

And then a second question on 850. I was just – we were just looking through your corporate deck. And I think on one of your slides in the deck you noted that there's additional indications under evaluation for that drug. Can you maybe talk – is there something outside of melanoma, prostate and triple-negative breast that we should be thinking about there? Thanks.

[Michel Detheux, President and Chief Executive Officer]

Hi, Chris, thank you for the questions. I'm going to start with the update about the data and I will let Joe continue about additional indication under consideration. And our next update on inupadenant will include the monotherapy expansion with six patients in each of the following indication; melanoma, prostate, lung and endometrial cancer, and the biopsy result for more than 20 biopsies in patient who are taking monotherapy. A collision between clinical benefit and a potential biomarker would be an important discovery in I-O field and expanding data on 50 PK/PD is important to move forward in our combination strategy.

We believe that disclosing data now will appear the next step for our inupadenant program. What we are planning to do later in the year is to go into more detail with the data related to the biomarker and explore with domestic inspections that will be level one useful for shipping our clinical strategy. And I will stop here for the data disclosure that we’re planning to do and turn to Joe for the additional indication that could be under consideration.

[Joe Lager, Chief Medical Officer]

Thanks, Michel. Chris, as we are considering other indications for this program, there are a couple of solid tumor indications that we are quite interested in, non-small cell lung cancer. As Michel said we involved some additional patients in our monotherapy cohort and endometrial cancer are both two types where we are considering doing a further extension.

[Chris Raymond, Piper Sandler]

Okay. If I can ask a follow-up then also – as we're talking about other indications, I think you've also in your prepared remarks on 448, I think I heard guys talk about gastric and pancreatic cancers as possible targets. When would you guys be able to make a decision on these tumor types? And what's gating in terms of – gating factors I guess in that?

[Joe Lager, Chief Medical Officer]

Yes. So I did mention that we are considering gastric cancer and pancreatic cancer. There we are evaluating the opportunity to cancer study designs. I would say we can likely provide an update on the development program later this year.

[Chris Raymond, Piper Sandler]

Thank you.

[Operator]

Next question is from the line of Daina Graybosch of SVB Leerink. Your line is now open.

[Daina Graybosch, SVB Leerink]

Hi, thank you for your question. This is Daina. One follow-up to the question you just had now on your development plan, they have evolved a bit over the years and I wonder if you could help us understand the rationale for the current plan and what you're looking for to make decisions going forward into the next six months, and whether in pancreatic you're still considering the combination with your A2A inhibitor, inupadenant and TIGIT, or this is more about purely TIGIT?

[Michel Detheux, President and Chief Executive Officer]

Joe, please.

[Joe Lager, Chief Medical Officer]

Thanks, Daina. So in terms of the rationale for our development plan, we are – and I think your question was focused on the EOS-448, the TIGIT program. So I'm going to focus there and you can follow-up on if you have questions there as well. So we are developing in non-small cell lung cancer that has always been an interest for us. We did have some debate over whether to proceed first the first-line setting with non-small cell lung cancer, or to look at it earlier adjuvant type of setting. We decided that the first-line setting provides us the opportunity to have data that we can compare more easily with our competitors and potentially provide a faster report in the adjuvant setting. So we prioritized that.

Head and neck cancer, I think there has been interesting indications for us for quite a while. We think that the biology there is quite similar to non-small cell lung cancer and anticipate that adding an anti-TIGIT to pembrolizumab therapy there should be a benefit to patients. This is indication where we feel like we have the opportunity to potentially catch up with competitors that are ahead of us who are maybe not being as aggressive in head and neck cancer as they are in other tumor types. So those are the reasons why we're interested in other indications.

We're interested in melanoma because we think being able to show activity in enhanced tumor after PD-1 therapy would be quite interesting. We're encouraged by the response that we saw in dose escalation in the patients who had acquired resistance to PD-1 after having quite long therapy on PD-1. And we've also seen a signal with inupadenant in checkpoint inhibitor resistant melanoma. So we are looking at that combination in that setting with the potential that that combination could benefit other patients in the post-PD-1 setting.

And then we have myeloma, we've generated data to show that with a collaborator at the Fred Hutchinson Institute in Seattle to show that TIGIT is really a much more relevant immune target in that type of cancer than PD-1 is, and have these pre-clinical proof of concepts that you see activity with an anti-TIGIT antibodies in a model of myeloma with the potential for additional benefit in combination with IMID.

In terms of the other indications for considering, particularly around pancreatic cancer that is something that we're continuing to think about as you know it is a tumor type where the historical success rate has been low. It's a challenging tumor to treat. But we do think it's quite interesting and we are still interested in the combination with our A2A receptor antagonist. There has been some recent promising data for other targets in the adenosine pathway in pancreatic cancer. It’s still very early data, but yes, we do think that combination could be interesting there. I'll stop there and see if I've answered your question, or do you have any follow-up?

[Daina Graybosch, SVB Leerink]

That was very helpful. And maybe a follow-up that's on a different topic around your biomarkers, your biomarker for inupadenant. Maybe you can remind us as context I know some competitors have developed adenosine signature. And can you remind us what’s in that signature? And if you're seeing something different and it sounds like you are, what you could be seeing something different than others have seen? And thank you very much.

[Joe Lager, Chief Medical Officer]

Yes. Thanks. That's a good question. So in terms of biomarkers, in our studies, both studies focusing on the inupadenant or EOS-850 A2A program, we are doing immunohistochemistry for immune cells as well as various targets within the adenosine pathway, so the A2A receptor and enzymes that produce adenosine, and we are also doing NanoString RNA profiling to evaluate potentially gene signatures. So in terms of what we are seeing as indicated by the title of our ASCO abstract, we think that there is a potential correlation between the expression or cells expressing the A2A receptor in the tumors and the clinical outcomes of patients.

The A2A receptor IHC assay was quite difficult to develop. It is a challenging target to generating antibody [indiscernible] A2A receptor. And it took our team quite a bit of effort to be able to develop that assay and then turn to it [indiscernible] testing for it.

So as far as we know, others, haven't looked at the expression of A2AR within the tumor as a potential correlate with patient outcomes. So that may be why we're seeing something unique here. It may also be because we have a very selective A2A receptor antagonist, whereas a number of the other identity receptor antagonists that are under development are less selective, target other receptors of adenosine.

In terms of the gene signatures, the adenosine gene signatures that people have reported on, we do have those gene in that signature, in our monitoring profiling and we will be looking at that. Mainly that's looking at – if you put adenosine in the system, what genes come up and they're mainly genes that are related to myeloid cells that are in that signature that's been reported in order to it.

So it is a way, I guess of looking for tumors that have a higher concentration of adenosine. Some may know adenosine is quite difficult to measure, because it has a very short half-life. So it's challenging to just go in and do a biopsy and identify whether a tumor has a high adenosine concentration or not, there is a target for adeno and we will be looking at that as well with our gene signature.

[Daina Graybosch, SVB Leerink]

Very helpful. Thank you very much.

[Joe Lager, Chief Medical Officer]

You're welcome.

[Operator]

Next question is from the line of Anupam Rama of JP Morgan. Your line is now open.

[Anupam Rama, JP Morgan]

Hey guys, thanks so much for taking the question and congrats on all the progress. I was also actually flipping through the corporate deck and on the A2A program and EOS-850 here, saw comment in the deck about a new formulation entering Phase 1 , any color here or tidbits you can provide. Thanks so much.

[Michel Detheux, President and Chief Executive Officer]

Joe please, can you update anything about the status of our new phase – the Phase 1 of a new formulation.

[Joe Lager, Chief Medical Officer]

I'd be happy too. So the formulation that we initially brought into clinic was a freebase formulation. We now have a salt formulation that we think could improve some of the properties of the drug in terms of dissolution at high pH. So we are moving forward with a clinical trial of that new salt formulation and are anticipating that we'll start in the coming months – coming couple of months.

[Anupam Rama, JP Morgan]

Thanks for taking our question.

[Joe Lager, Chief Medical Officer]

Thank you.

[Operator]

Next question is from the line of Arthur He of HC Wainwright. Your line is now open.

[Arthur He, HC Wainwright]

Hey, good afternoon everyone and thanks for taking my question. I had a two question in regarding the adenosine antagonist program. So first seemed like the AstraZeneca and Arcus are more focused on triplet combo for the CRPC. And could you guys give us more color on your confidence on your molecule for a triplet, duplet or even monotherapy for – in that indication?

[Michel Detheux, President and Chief Executive Officer]

Hi, yes thanks for the question indeed, well, we believe that doing immunotherapy will help us to get a better understanding of the mechanism of action of adenosine receptor antagonists in prostate cancer. And that could also help us to identify a specific population that would be more adapted to such treatment. And then this is – I would say the dimensional for giving monotherapy and we are currently at the end of the Stage 1 of this monotherapy expansion.

For the combination, the combination with pembrolizumab is additional added value. It would allow to explore, I would say treatment, which is chemo free, which has also have significant expectation from the patient with prostate cancer and could help us to differentiate our program compared to competitors. Joe, do you want to add something for this strategy in prostate cancer?

[Joe Lager, Chief Medical Officer]

Thank you so much Michel.

[Arthur He, HC Wainwright]

Thanks for that. And my second question is regarding the pipeline. So what can we expect from the pipeline targeting the adenosine past, I believe you guys up into announce the additional candidate in later this year?

[Michel Detheux, President and Chief Executive Officer]

Yes, indeed. Based on the characterization of inupadenant, our research team has identified a new target, which has never been described as [indiscernible] pathway for cancer immunosuppression. And we have been excited with this new target that is both of interest to go for a while to refer other standard of care and to be also used in combination with inupadenant and A2A. We continue to make progress on the identification of the clinical candidate. And we are planning to report this clinical candidate before the end of the year and move forward in a IND enabling studies thereafter.

On top of this adenosine pathway program, we are also planning to add additional programs in our pipeline, as I said that will be complimentary to TIGIT and A2A receptor programs and will allow to adeno transition mechanisms of immunosuppression.

[Arthur He, HC Wainwright]

Thank you. Thank you for taking my question.

[Michel Detheux, President and Chief Executive Officer]

Welcome

[Operator]

[Operator Instructions] Our next question is from the line of David Nierengarten of Wedbush Securities. Your line is now open.

[David Nierengarten, Wedbush Securities]

Hi, thanks for taking the question, a bit of follow-up to Daina's, when you think about your assay or thinking about assay in tumors for A2A receptor expression, I guess the question is thinking about the competition one, how proprietary can you protect your assay to use with your – with EOS-850?

And then two, are we going to see or have you seen a situation where I guess not a 100%, but 70% or something majority of tumors express the receptor in your hands and so a competitor could potentially just say, I'll focus on that tumor, seeing your results and go after that. I'm just curious, how you see if your assay, if your research here provides you a competitive edge on the development. Thanks.

[Michel Detheux, President and Chief Executive Officer]

Hey David, thanks for the question. As mentioned by Chris in his former questions timing to discuss our data was also related to the protection of how that turns on any patent application. And we've been able to the best extent to protect this new, I would say biomarkers related to A2A receptor antagonist. As Joe mentioned it’s been a significant challenge to be looked when the assay that will be robust to be used with clinical samples.

And we are very confident that we'll be able to use this assay at large scale. We are still working on additional data because this assay also give us, I would say insight into a making distraction that is never been described so far for adenosine receptor antagonist and we see the reason why we disclose additional data later in the year or next year.

In terms of the application and the percentage of participation, I would like to turn to Joe and get additional comments to explain why we believe that it will be a competitive advantage for iTeos

[Joe Lager, Chief Medical Officer]

Thanks, Michel. So we are continuing to generate data on the use of pathway. We are looking at the number of cells within the tumor expressing the A2A receptor. So that's a continuous variable. So we're continuing to work on what is the cutoff and what would be considered high and what would be considered low. And we're using the information that we have to interrogate the expression in different tumor types, because this has been such a challenging assay to develop. There's not a lot of data out there available to say what the expression is this A2A receptor by IHC in different tumor types.

So our lab has been working on that and we have some internal data there, but I think it is a competitive advantage because we've at least had a head-start on doing these assays and understanding expression in different tumor types.

[David Nierengarten, Wedbush Securities]

Okay. Thank you.

[Operator]

I'm showing no further questions in the queue at this time. Ladies and gentlemen, thank you for participating in today's conference. This does conclude your program and you may now disconnect. Everyone have a great day.