Compugen Ltd. (CGEN) Earnings Call Transcript & Summary

Good morning, everyone, and welcome to Compugen's COM701 in ovarian cancer and UNIGEN platform update event. [Operator Instructions] Before handing the call over to the company, please review the forward-looking statements on this slide. I'd now like to introduce Dr. Eran Ophir, President and Chief Executive Officer of Compugen. Eran, please go ahead.

Good morning, everyone, and thank you for joining us. I'm Eran Ophir, President and CEO of Compugen. Today, we'll provide a brief overview of Compugen's key value drivers discuss the clinical opportunity for COM701, our first-in-class anti-PVRIG antibody being studied as maintenance therapy in second and third line platinum-sensitive or brain cancer and share an update on the continued evolution of UNIGEN our AI-powered discovery platform. Dr. Oladapo Yeku, the lead investigator on our Myron adaptive platform trial from Harvard and Mass General Hospital, will share his perspective on the evolving treatment landscape in ovarian cancer, setting the stage for the interim analysis of the MAIA study with PFS readout that is expected to be reported by Q1 2027. Later on, Dr. Sharon Pedroso, our Senior Vice President of Research and Discovery will discuss how we're expanding UniGen's capabilities to support Compugen's next generation of immuno-oncology discovery. While we will not be disclosing any new targets today, we believe it is important to keep you updated on the capabilities we are building in this area of high unmade. Following presentations from Dr. Eco and Dr. Frederuso; Dr. Michel Miller, our Chief Medical Officer, will join us for the Q&A session. So let's get started. This slide highlights Compugen main value drivers today, all rooted in our discovery capabilities and derived from our AI-powered computational target discovery engine called Unge. First is COM701, our wholly owned potential first-in-class anti-p-verG antibody, currently being evaluated as maintenance monotherapy in second- and third-line platinum-sensitive ovarian cancer in the my ovarian adaptive platform trial, which Dr. Yeku will focus on. Second, is Comnethe TIGIT antibody discovered following our computational identification of TIGIT in 2009. Come 2 became the TIGIT component of AstraZeneca's bispecific antibody will vogostamite that AZ is currently evaluating in 12 Phase III trials. Compugen is eligible for up to $195 million in regulatory and commercial based milestones and up to mid-single-digit royalties on ostomy. Which AstraZeneca has previously projected to have peak year nonrisk-adjusted revenue of over $5 billion. Third, we're advancing GS-0321 formerly COM503, which was licensed to Gilead in 2023. This program also originated from our computational discovery platform UniGen. GS-0321 targets the iLet binding protein and represents new and cool approach to cytidine biology for the treatment of cancer. Today, we have received $90 million from Gilead, $60 million upfront and $30 million upon in the acceptance. And remain eligible for up to an additional $758 million in development, regulatory and commercial milestones and single to low double-digit royalties on worldwide future net sales. Altogether, these programs and partnerships validate Unigen as an engine for identifying novel immuno-oncology drug targets. UNIGEN discover targets currently make up our undisclosed research pipeline and to our expanded capabilities, we are working to continue to bring more innovative molecules into areas that unmet need for patients with cancer. With that broader context in mind, let me focus on COM701, our most advanced wholly owned program and why we believe PPG inhibition is relevant in ovarian cancer. In this slide, we summarize this biological rationale, including the unique dominant expression of Pipa on stem-like memory T cells, which is different from other checkpoints like PD-1 and TIGIT. Therefore, by blocking PVRIG, COM701 is designed to alter the tumor environment, including in less implant tumors such as brain cancer. Accordingly, we have observed antitumor activity of COM701 in patient populations, typically less responsive to conventional checkpoint blockers like PD-1 negative or brain cancer. So what is typical for new drugs, we begin our COM701 clinical trials in heavily pretreated platinum-resistant ovarian cancer patients. In these early trials, COM701 in monotherapy and combinations induced clinical benefit and durable responses regardless of PD-L1 status. As you can see here, in these tourist bars, that represents clinical benefit in patients with PD-L1 negative disease. Importantly, PD-L1 negative, platinum-resistant to bari cancer patients historically showed 0 overall response rate. even when PD-1 and TIGIT blockade were tested in highlighting COM701's unique mechanism of action. In addition, we identified retrospectively, that patient without ever metastasis, appeared more likely, as you see here on this slide, almost 40% to benefit clinically from COM701 even in these advanced settings. These observations informed the myovarian design, where we decided to enrich for patients more likely to respond to COM701, but going earlier in the treatment algorithm on the very right side of this graph, heavily pretreated platinum-resisted brain cancer patients into the second and third line maintenance settings. We select patients with no liver metastasis. The revenue system is less compromised by multiple rounds of chemo and they have low tumor burden as we select only patients that responded to the last line platinum chemotherapy. These patients have an unmet need for a drug with strong safety and durable antitumor activity to prevent or delay tumor recurrence following response to platinum-based chemotherapy. So the milovan is designed to evaluate COM701 monotherapy against placebo in these defined maintenance settings with 40 patients randomized to COM701 and 20 to placebo. This go to determine whether COM701 can extend the period of platinum sensitivity, delay progression to platinum-resistant disease and help preserve future treatment options while maintaining a tolerable safety profile for patients in the maintenance settings. As mentioned, data from this trial is expected to be reported by Q1 2027. With that context, I am pleased to turn the call over to Dr. Yeku from Harvard University and Mass General Hospital. Dr. Yeku will share his perspective on the evolving treatment leap in ovarian cancer and rationale for evaluating COM701 in these Internet settings. Dr. Yeku, the floor is yours.

Hello, everyone. Thanks for this opportunity to share some of my thoughts about the evolving landscape in the management of ovarian cancer. Next slide, please. So when we think about ovarian cancer, it's helpful to understand the patient journey, basically thinking about how patients move through and how we think about the goal of therapy at each setting. So generally speaking, when our patients present with advanced disease on diagnosis, we use a combination of chemotherapy and surgery, either before or after each other with a reason new adjuvant version or an adjuvant version. And depending on the patient's genetic findings, they may be eligible for maintenance therapy. And our goal in this initial treatment strategy is to cure the majority of patients. Unfortunately, some of our patients will recur with disease. And depending on their nestologeostage, at least in every case is something that happens more often than we would like. And this period of remission is defined by the time of platform sensitivity, which I'll talk about in a minute. But the longer it takes for the case to come back, the better. However, the bottom line is that the majority of patients, they will have relapsed disease and understanding and developing therapies that are both efficacious and also preserve quality of life is this setting is what's most important. Next slide, please. As I mentioned before, the way we delineate or distinguish recurrence or relapsed is by platinum sensitivity. The current definition of this is the time from their last carboplatin or cisplatin exposure. If it's greater than 6 months, that's the PFI, the platform free interval, then they are thought to be platinum sensitive. If it's less than that, they are thought to be platinum-resistant. Eventually, most patients who develop platinum-sensitive disease will eventually develop platinum resistance. So you can imagine that a patient is treated -- about a year later, the disease recurs as platinum sensitive. They get another platinum doublet combination that may work for a time. If it works for greater than 6 months, then they're still platform sensitive. But unfortunately, over time, that platinum-sensitive free interval will decrease and all patients who are platinum sensitive will become platinum resistance. And even though this timing seems particularly arbitrary as it is time to the carboplatin exposure, it does have biological significance. We know that patients who are in the platinum-sensitive stage of the digital platinum stage state of the disease have more options. Their survival is longer. Patients who have platinum-resistant disease now have multiply treated cancers that are continuously evolving -- and in those particular settings, the mortality is higher. But again, it's on a continuum, if you will. We have more options for platform sensitivity or platinum-sensitive disease. There are fuel options for platinum-resistant disease. But for a long time, in ovarian cancer, there has been a lot of work into understanding why there is a dichotomy in patient outcomes for these and what strategies we can use to extend platinum sensitivity, both biologically and also clinically. And many of our efforts so far have not been successful. In the past, we'd use chemotherapy, pazopanib, all sorts of things, but we have not been successful, constantly highlighting that this is a goal. There is one medication that we'll often use in this platinum-sensitive setting, and that's bevacizumab. And the goal of bevacizumab is where we combine it with the platinum doublet, we can then continue it as maintenance, providing an option for patients that's reasonably tolerated even though it has some side effects, I will talk about later. But in some patients, it extends that platinum-sensitive window, so they did not become partum resistant and have to deal with all of the equity that comes with that. Next slide, please. So one of the key goals of patients who have recurred from a solid tumor perspective is that we know that these patients are to lower curable. So treatment selection, including maintenance options, becomes a balance of both toxicity and efficacy. We want to control the disease. We want to prevent progression of the disease. At the same time, we want to make sure patients preserve their quality of life. I just mentioned the role of bevacizumab being one of the agents that we use in this platinum sensitive and even in the platinum-resistant setting, but there are many patients who are ineligible for bevacizumab. So for example, some patients may have received it with their upfront treatment and their cancers progressed while they were on it. Many patients have absolute contraindications. They might have fistulas or they might have high blood pressure. There's a long list of medical reasons why bevacizumab might not be suitable for a patient. In addition, their quality of life side effects that we see with this drug, such that some patients elect to not take bevacizumab and undergo observation. Again, with the understanding that the cancer will progress at a certain time, but they value their quality of life in the current moment. So they go that route. So for patients who are eligible for bevacizumab, it's something we discuss and we offer as maintenance, we get it with the chemo and then following the chemotherapy. But for some patients, observation is the way to go because again, it preserves that quality of life. And the way we follow these patients is with periodic or regular clinical exams. We do scans about every three months or so, but it varies on clinical practice. Again, because we know the inevitability of disease progression once patients have suffered a relapse. Next slide, please. So to fill this space, knowing that bevacizumab might not be appropriate for some patients and knowing that even patient preference might skew you away from bevacizumab. And knowing that the idea of observation is something that patients might need to default to. We've continued to do research into trying to understand what other therapeutic modalities we can incorporate into this platinum-sensitive space to prolong, again, that platinum-free interval or decrease the time it takes for disease to progress. And one drug category that's moving into the space are antibody drug conjugates, either as monotherapy maintenance or in combination with bevacizumab. Now there is no doubt that antibody drug conjugates are effective. We have lots of efficacy data in the platinum-resistant setting, this is where these drugs are. And they've really reshaped the way we think about immotherapy and therapeutic sequencing in this space. So that's in logic that if they work in the platinum resistance study, we need to move them up to the platform sensitive setting, either with chemo and/or as maintenance is something that is actively being pursued in clinical trials, it's also too early to tell. We've had at least one study that showed no real difference in terms of progression-free survival. But this was using a different type of ADC, there are newer ones that are being tested, and those results will be seen soon. The one thing we do know is that adding an antibody drug conjugate either with devacizumab cells increases side defense. That is the one guarantee we have. And we know this because these drugs have a well-defined toxicity profile that we've learned from the platinum-resistant setting. So for patients who are still trying to avoid toxic option as maintenance, they're still going to have the same problem. So we will buy some efficacy because ADCs work similarly to chemotherapy will come at a cost of increased adverse events. Another issue is that the vast majority of our ADCs have a topic summaries on payload. And currently, there's a debate in the field that because most of the ADCs we have at tours1 inhibitors, if we use them in the platform sensitive setting as maintenance and the patients progress or relapse. Now they are coming in with increased toxicity burdens, maybe pablum resistant disease, and the best treatment we had, which are the topo1 ADCs have not been expanded as maintenance which some people feel is perhaps not the best way to deploy or utilize this medication. Now that said, there's research going on both sides of the fence to better understand this. So their Os and cons are certainly notable reasons for why antibody-drug conjugates may not be the appropriate choice for all patients as a maintenance treatment, especially in the platinum-sensitive setting. Next slide, please. So before we go into why COM701 might be an option in this setting, it is also worth mentioning that some of the other maintenance treatments that we've tried in the past, including PARP inhibitors have since been withdrawn for this use by the FDA, in the second-line setting, but in case some people were not familiar with that, in the past, we used to do or give PARP inhibitors as maintenance with or without bevacizumab, most of the time without, and this is because these drugs have their own toxicities. And what we found was it didn't go initially, they appear to be healthy. When we looked at overall survival and we looked at the burdens of toxicity from these drugs, they ended up becoming detrimental in some cases and in effect, in many cases, and that has since been withdrawn. So currently, anti-angiogenics like bevacizumab or what we have antibody drug conjugates, have closing cons with the most recent data we have showing that they're not efficacious as maintenance therapy. We need new options. One of the advantages of COM701 as an immune checkpoint inhibitor is its tolerability profile. So we have some data in the platinum-resistant setting about its preliminary efficacy, and there will hopefully be a public report or management to this effect soon. But one of the highlights of this drug was that we found that there was a subset of patients who, based on the mechanism of action of this drug, we're having responses and durable responses without toxicity. And as I mentioned before, the absence of toxicity is a highly, highly priced asset in patients who are looking for maintenance therapy because they've had chemo. So the Copa deal the disease and what they're looking for is something that can extend that benefit that is also compatible with the quality of life. So a key advantage of COM701 is that the know very well that it's very well tolerated, and we know that it can provide a long progression fee survival in select patients. And these characteristics make it a suitable come to be evaluated as maintenance therapy. And because we're using it earlier on in the patient's journey before they become all of our data currently become COM701 is in the platinum-resistant setting. We know that these patients are fitter, both clinically and also immunologically, there's a lot of data in ovarian cancer and other solid terms that the more chemotherapy we expose to our patients that physical reality that we see in the clinic and that decline, there is also an immunologic reflection of this as well. So for several reasons and the ones I highlighted, looking at an immune checkpoint inhibitor than COM701 and the platform sensitive setting becomes something worth pursuing. Next slide, please. So the question that becomes to what end. Immune checkpoint inhibitors have been studied extensively for GYN cancers with mixed benefits, and it was not so recently that we got our first approval in the platinum-resistant setting with chemotherapy, for platinum-resistant ovarian cancer. The key goal in the second or third line platinum-sensitive recurrent setting is to maintain that platform sensitivity because if we have a drug or a therapeutic that's reasonably tolerated, low side effect is not chemo like an ADC or chemo-like, like an ADC and extends the patient's platinum-free interval, then we've kept them in that box that I showed you a few slides ago in that platinum-sensitive setting. This allows them in the future if they progress to be rechallenged with the platform agent, a platinum doublet. And these patients can stay in that physiologic or biologic or clinically defined box. So providing a drug or a treatment that has low toxicity is important, providing a drug that maintains platinum sensitivity is important. And inevitably, the longer a patient stays in the platinum-sensitive box, the longer it takes them to progress or evolve into the platinum system box, the more we can perhaps benefit our patients in the long run. So to briefly recap, the goal of COM701 studied as a maintenance after platinum doublet therapy in patients with second- or third-line relapse atom sensitive ovarian cancer is to provide a clinically meaningful well-tolerated option for patients who might not be eligible or intolerant to bevacizumab, which is the current treatment with the hopes that this agent will prolong their platform free interval, keep them in that pipeline sensitive state and also provide them adequate quality of life at a time when their immune system can be meaningfully engaged.

Thank you, Dr. Yeku. As a reminder, Dr. Jake will join company management for the Q&A portion of our call. At this time, I'd like to introduce Compugen's Senior Vice President of Research and Discovery, Dr. Sharon Kratos. Please go ahead.

Good morning, everyone. Thank you for joining us today. My name is Dr. Sharon Cardoso, and I'm the Senior Vice President of Research and Discovery at Compugen. I'm excited to share today an important capability we have built based on our established discovery engine. We believe this capability has the potential to bring value to areas with high unmet needs. As discussed earlier today, over the years, Compugen's discovery platform has generated multiple assets. Some programs are in early stages of discovery, some in clinical developments and several are being advanced through strategic partnerships. But what is the engine behind all these discoveries. Behind all these discovery stands Uniden our AI power discovery engine continuously connecting computation, biological validation and clinical learning. At the center of competent approach is our proprietary knowledge base. This is a computational engine, which is actually a collection of specialized AI-powered computation approaches and algorithms that are designed to study very complex biological systems. These algorithms prioritize hypothesis based on their therapeutic potential and select the right tools that are then applied across multiple data types. The discovery engines output a potential novel immuno-oncology targets that are expertly validated, resulting in the therapeutic drug candidates that have over the years entered the clinic. Clinical trial data that generates an additional layer of information that fits back into our database and supports all our future and ongoing discovery efforts. It is this established engine that we are now expanding into a new opportunity space called the tumor-associated antigens. Tumor associated antigens provided to more address to the target therapies, directing the drug activity or delivery specifically to cancer cells while sparing the healthy ones. Bispecific antibodies engineer with one binding arm to the tumor anti-channel while the other arm brings the modality. TAA plays a central role in many of today's promising cancer therapy modalities. For T cell engager, the TAA brings the T cells into direct contact with the tumor cells. For other targeted immune activation approaches, it may mean the tumor selective activation of the immune pathway, and beyond immune engages for other targeted modalities such as ADCs, the TAA enables the local delivery of the therapeutic drug directly to the tumor cell sites. And across all these modalities, the target determines where the therapy goes and where the biological activity happens and as a result, the TA quality can directly influence both efficacy and safety. And that is exactly where one of the larger unmet need lies in the field today. the need for novel and selective DAAs. Focusing now on T cell engagers, which have emerged as one of the most exciting modalities in oncology. A bispecific antibodies used to bring the T cells in close proximity space to the tumor cells, resulting in their direct killing. This powerful modality has attracted substantial industry investments and growing market opportunities in recent years. However, the power of this high immune activation model also highlights a fundamental challenge. A cell engager can only be as selective as the antigen directing it. And only few TIAs have the right profile, optomispecificity lower healthy tissue exposure and high tumor coverage. As of today, 12 T cell engager drugs have been approved, validating this therapeutic modality and yet only two in solid tumors where target quality is still a critical constraint. The figure below shows how we look at target profile signal across healthy tissues where red means high level in the healthy tissue and green means a low level. One example of a clean target is DLL3. The approval of talatumab in small cell and cancer targeting this antigen demonstrates our favorable clean target profile can help to unlock the potential of the therapeutic modality. You can see how DLL3 is exceptionally clean with no rate issues at all. meaning it is mostly absent from the normal healthy tissues and expressed almost only on the tumor cells. On the other hand, mesothelin is an example of a different type of target. You can see here that the target is quite clean, beside the red, it means high expression level in the healthy lung cells. As a result, the development encountered dose-limiting toxicity of on target of tumor meaning activity outside of the tumor and the healthy line that is data associated with its normal high lung expression of the TAA. And actually, many target this extensive normal tissue expression. As shown here, while others display different restricted pattern and the TA selection, but the right indication has become a challenging task. As we believe that the powerful therapy is only as good as its target, we have expanded our established capabilities and target discoveries to build UniGenc, a dedicated engine for TAA discovery. We built upon our proven foundation of Compugen's knowledge base and combining biology, computational and clinical validation. We start with the knowledge base and up from definition of the target desired profile. Then specialized AI-focused discovery tools, integrate multiple layers of biological data simultaneously, spanning different OMC types. Moving to the output platform, first, generate explainable target scoring. This prediction then undergo extensive TI-specific experimental validation, including minister chemistry, normal tissue exposure, functional toxicity assessment resulting in the drug candidates. And ultimately, the output delivers differentiated opportunity, novel TAA, Nova drug candidates and patient selection, matching the targeted therapies with the right patient population based on biomarker target expression. But how do we find the right TAAs? As said, finding the ITA is a major challenge. Our approach is differentiated in several ways. First, it is a multidimensional approach. A target is evaluated broadly and deeply using genomic data, balcony sequencing, single-cell transcriptomics, proteomics and special biology and is assessed based on multiple parameters together. This is a versatile discovery platform. We match the defined criteria to the desired specific modalities and the analytical approach to the biological questions, which opens opportunity across targeted modalities. And this deep biological understanding and explainability allow us to identify opportunities that may remain invisible when viewed to a single data set, enabling us to uncover novel targets with the aim of translating them into a clinical stage therapeutics. So how either multidimensional multiomics approach, allowing us to achieve this specificity and understanding and our discoveries. First, we start with search broadly. This means giving our algorithm access to a very rich biological landscape. The platform integrated information for more than 100 million single cells across multiple cancer subtypes, over thousands of tumor and normal proteomic samples in a proprietary enormous at Atlas is composed of multiple tissues and over 100 healthy cell types. We believe that the data scale, however, is not enough. And understanding deeply means creating a multiparameter target profile for every target candidate. We assess tumor specificity, patient coverage, normal tissue exposure heterogeneity and then calculate the potential therapeutic index. That integrated assessment is a defining element of GenX used for an informed TAA selection. We integrate these multiple biological layers into explainable target scores. The graph shows two major scores the platform produces. Predicted efficacy or activity on the Y-axis and predictive safety or toxicity on the X-axis with each dot representing a potential TAA, in this case, in colorectal cancer. Zooming in now on a specific target A that we have discovered with a very high scores in efficacy and safety. The figure on the right illustrates the multiple parameters contributing to the total score. Divided into different features that originate from the different Omics data types, allowing us a deep understanding of the biological profile of each potential target relative to benchmark TAAs. This allow us to adapt each scoring system to the desired modality in its requirement. And importantly, it enables stronger hypothesis and the ability to identify target with potentially better profile than benchmark. The deeper understanding is not only the scoring system as we perform deep validation on every feature and here is how the data look like. Evaluating multiple parameters such as RNA expression profile, the cellular resolution of the different cell types and the protein membrane level in both normal and tumor tissues. And importantly, we experimentally validate each target localization to immunochemistry to identify tumor specificity across patient cohorts. Individually, we believe looking at each layer separately gives only partial information. But together, we believe that they build the confidence in the target differentiated biological profile. And indeed, we have several target candidates that have been prioritized for further experimental validation in our early pipeline. But what if we could expand the TAA discovery space beyond a single TAA. We believe the target pairs can expand the TI discovery opportunity. It is important because some therapeutic challenges may be addressed more effectively to paired targeted approach. In an negated strategy, two targets, A and B, must be present together on the same cancel. The goal is to improve selectivity and sparing the healthy tissue. Therefore, the T cells will only kill in the presence of both targets on the tumor cell and will not kill the healthy cells expressing only one of the targets. In an rated strategy, either Target C or Target D can support killing activity of the tumor cells. The goal here is to broader tumor cell coverage within the patient and overcoming potential resistance mechanisms of down regulating or mutating single TAA. On the graph below, lightly represent the tumor cells, while dark blue represents the healthy sales. The top two rows show the expression of each individual target, Target A on the top and target to be in the middle. While the bottom row shows their combinations. As shown upon dual targeting of target and target fee in an end gated approach, tumor selectivity is improved, sparing the healthy tissue. The example on the right represent an or gated approach from prostate cancer, demonstrated combining Target C on the top, Target D in the middle and either target or target in the bottom improves the coverage of tumor cells within the patients. We believe these approaches could significantly expand the discovery space from individual targets to rational target combinations that may create opportunities that cannot be addressed by conventional single target discovery approaches. To summarize what we have discussed today, we started with Compugen's validated Discovery Foundation and Unigen, with a track record of identifying or immuno-oncology targets as discussed earlier today and translating them into the clinic. On the right is Unigen expansion of this foundation into new and broadly valuable space that include novel TA discoveries, to create differentiated opportunities for multiple targeted modalities such as T cell engagers. But ultimately, our goal is to make a meaningful difference for cancer patients. First, we believe that a scalable discovery engine has a potential to generate multiple TAA driven opportunities across solid tumor indications and modalities. We believe these discoveries could support future potential partnerships. And finally, discoveries from our platform can potentially be combined with our current ongoing early programs. To conclude, we have created an expanded target discovery engine across I/O field to support the next generation of targeted therapies. With the aim of achieving clinical meaningful therapeutic effect for unmet cancer indications. Thank you very much for your attention. With that, I'll hand back the call over to our operator who will take us through the Q&A portion of our event.

Great. Thank you, Sharon. So yes, at this time, we'll be conducting a question-and-answer session with our speakers. [Operator Instructions] We're going to begin with two questions we received over the webcast. So the first one is, what is your platform's differentiation versus competitors, other companies looking for new TAAs?

Sharon, you want to take this one?

Sure. Thank you, Tara. As discussed today, we are taking a broad multi-dimensional and multiomics-based approach together with a very deep logical rationale understanding -- we are not looking into a single layer of data sets, but we are looking on multiparameter multidimensional understanding of the tumor and the biology. Another aspect is that we built upon UNIGEN Foundation in the IO field and the vast attests that we have mitigated and digested over the years at Compugen.

Great. Thank you, Sharon. On the next question, what would be your first modality to focus on and why?

As mentioned earlier, we can use at discoveries for any desired target modalities, for example, antibody a conga that brings the drug. But our first focus is on T cell engager and targeted immune activation as we believe in the power of immune activity that can be directed specifically to cancer cells, assuming we have the right AI to select or the combination.

Great. Thank you, Sharon. So our next question will come from Stephen Willey at Stifel.

Yes. Can you guys hear me okay?

Yes, we can.

Perfect. Maybe a question for Dr. Yeku. I know that we've seen some attempt at leveraging immunotherapy within platinum-sensitive, maintenance. I think with some differing results. How do you think the mechanism of COM701 has the potential to change the narrative around the use of maintenance immunotherapy? And then maybe a question for the company. Just curious how you plan to leverage this discovery effort into TAAs? And is this something that you would look to build out your own internal pipeline or do you see this more as an opportunity for various collaborative partnerships?

Yes, for sure. I can tackle the first part of that question. I think a lot of our efforts so far with immune checkpoint inhibitors as maintenance therapy for ovarian cancer Much of that stems from our understanding of the role of PD-L1 as a biomarker and this was way back end. I think now it's better understood that this marker is not the most reliable one that we have because it's very dynamic. And many of these trials involve a combination of immune checkpoint plus chemotherapy followed by immunotherapy or immune checkpoint inhibitors by themselves. Again, our understanding in terms of the effects of chemotherapy or concurrent chemotherapy with steroids and everything else. And the potential kind of opposite effect that, that might have leading into maintenance, I think, is becoming better understood. There are a lot of trials now that are separating both of those things. So I think the PAR studies, one, because we weren't using an appropriate biomarker to because there were chemo plus I/O followed by IO, which is a different strategy here. Those are the two first reasons. The third and perhaps most important reason is that come works very differently than a PD-1 checkpoint inhibitor of EverPD-1 or PD-L1. The PD pathway has been shown to be specifically important in ovarian cancer, just in terms of the way it works, we have the endrytic cells and further down the line cytotoxic T cells. But I think more disease-specific mechanism exists for COM701 that doesn't necessarily or hasn't necessarily existed for immune checkpoint inhibitors targeting the PD-1, PD-L1 access. And because we've separated out the cytotoxic debulking phase of our plan from the maintenance phase, again, all of the issues that will be concerned about regarding the myelosuppression or immunosuppression we get from chemotherapy and steroids, that's already behind us without necessarily jeopardizing the debulking effect that we're getting with chemotherapy. So I think for those reasons, at least for me, it's reasonable to expect a different result than some of the other studies that we've done in the past.

Thank you, Dr. Yeku will take the second question about the utilization of the platform. either for internal pipeline or collaboration. I think that eventually, the way we always handle it. It was right for older assets. Some of them are in our pipeline. Some of them are being partnered and it's the same for Unit gen and neurogenic part. It really depends on what is right for the program. If we think that for the program, we can move it ourselves and bring value and take it to cancer patients in the right settings and bring it in the right pace and eventually bring value to our shareholders, we'll take it ourselves. If we think that there is a good reason why to partner and for different programs, it could be in different stages, then we could also partner. So I think overall, I would say what you saw from us in the past is also the plan for our next asset. Sometimes we've been partner, something we can move it ourselves.

Great. Our next question comes from Bill Ling at Leerink.