First, global vision on non-small cell lung cancer. Second, a more precise approach on what our lead product, Tedopi, can bring to this disease. Eventually, Alexandra will present the most recent data, ovarian cancer, with new initiation for us that was presented at ASCO very recently. Alexandra made an oral presentation at ASCO in Chicago a few days ago. In a few words, I would like to make a brief introduction on the company. This is a company I joined less than a year ago. I am absolutely convinced that this is a future great biotech company in France and in Europe, because we have incredible products. We have this product that we will go into details today, which is Tedopi. It is an immunotherapy, which is very promising with already more than 700 patients that have been treated. We expect to have a phase III readout early 2028. It is very close now. We have a second compound, which is lusvertikimab, which has delivered a positive readout in inflammatory bowel disease last year, in particular in ulcerative colitis. We are not going to elaborate on lusvertikimab today. This is not the purpose of this webinar. If we can share, Thibault, the first slide to give a brief overview of the company's pipeline. Of course, a forward-looking statement as we are a listed company. This is compulsory. On the next slide, you will have an overview of our clinical assets, which are twofold. We have proprietary assets, which are lusvertikimab and Tedopi, and some partnered clinical assets with Boehringer Ingelheim and Veloxis, which is part of Eisai, the Japanese company. As you can see, for lusvertikimab, we already have delivered phase II data in ulcerative colitis last year. We are now preparing a subcutaneous formulation that is more suited to the actual market, the actual needs of the patients. We are planning to launch rapidly now a second indication, which is some kind of subset of ulcerative colitis. The second indication is called chronic pouchitis. It has the potential to readout in 2027. We could imagine to launch a product in a few years. For Tedopi, the beauty of our pipeline is that we have this phase III ongoing ARTEMIA, on which Benjamin will spend some time. We also have a series of investigator-sponsored studies, in particular, the one that has been announced and described by Alexandra at ASCO on ovarian cancer. We will have additional readouts in the second part of this year, H2 of 2026, in non-small cell lung cancer in a larger population than ARTEMIA. We also have long-term readouts of pancreatic cancer trial. We will leave the floor to Stephen, who will give a vision on the pathology itself. Thank you so much to all of you, Stephen, Benjamin, and Alexandra, for taking the time to make these presentations that will hopefully give more insights to our participants. Thank you so much. Well, thanks for having me. My name is Dr. Stephen Liu. I am a thoracic medical oncologist at Georgetown University in Washington, D.C., where I'm the Chief of Hematology and Oncology and the Head of Developmental Therapeutics. What I'd love to do to set the scene for some of my colleagues is describe the current state of the treatment of lung cancer and how far we've come and really outline the unmet need. If we look at our slides here, I believe I start with some disclosures. In the past 13 years that I've been at Georgetown and treating lung cancer. We can go to the next slide. Past 13 years, we've clearly made a lot of advances in the treatment of lung cancer. We've really seen a wide reversal. Lung cancer is a fairly common disease. These are U.S. numbers, where you can see it's the second most common cancer in men behind prostate, the second most common cancer in women behind breast. If we click ahead, while it is the second most common, it is by far the most lethal. We click ahead to next. It's by far the most lethal cancer. You can see the number one cause of cancer-related death for both men and for women. As you can see, it represents more deaths each year in the U.S. than prostate cancer or breast cancer or liver cancer or ovarian cancer combined. It remains a huge unmet need and one of the most lethal cancers that we have. If we go to the next slide. Here we can see that in red on the left, we see the mortality for men and for women. Lung cancer is on the way down, fortunately, but still far outpacing any other cancer in the U.S. On the right there, you can see the initial stage of diagnosis. These are 2026 numbers. What we see as part of the reason is we detect lung cancer at a fairly late stage, with the most common stage in the U.S. being stage IV. Outcomes for stage IV, as one could imagine, are clearly worse. If we look at our survival numbers, while they are better for localized and regional, they're still fairly poor across the board. Our five-year survival rate of 28% pales in comparison to other cancer types. We look at breast cancer, five-year survival rate's 92%, prostate cancer, 98%. Colon cancer, a very important cancer, has a five-year survival rate of 65%, and at lung, we are at 28%. While we are proud of all the advances that we've made, and while these are the best survival numbers we've ever seen, we still have a long way to go, and this still remains an incredibly lethal disease. If we go to the next slide. We've seen advances in the treatment of lung cancer really in the form of two different paradigms. One is the development of targeted therapies following on the heels of the Human Genome Project, and the understanding that certain genomic subsets of lung cancer can respond very well to novel targeted therapies. Here we see real advances in medicinal chemistry, and if we can identify certain subsets of lung cancer, we can deliver very effective targeted therapies. Things like EGFR, ALK, ROS1. When we find these alterations, when we deliver a targeted therapy, we expect responses for the vast majority of patients. While there are some exceptions, for most of these patients, we will see resistance in one to two years, which remains a real challenge in the clinics. Importantly, this is only a subset of patients. For most patients with advanced lung cancer, immunotherapy will be the backbone of our treatment. This is appropriate for most cancers and across both histologies. For some, we use monotherapy, PD-L1 or PD-1 inhibitors alone, and for most, we use combinations, either dual immunotherapy or combinations with chemotherapy. Immunotherapy really is the mainstay for most patients with advanced lung cancer, and it's made a huge difference. Not only has it changed how we treat lung cancer, it's changed how we think of lung cancer and really raised the bar in terms of what is possible and what our expectations are. On the next slide, we get into some of the details regarding immunotherapy. KEYNOTE-024, I think, is one of the more important studies that changed our standard of care. This was a study presented at ESMO in 2016. In this trial, we compared a single immunotherapy agent, a drug called pembrolizumab, a checkpoint inhibitor and antibody targeting the PD-1 protein. This immunotherapy agent alone compared to standard chemotherapy. Chemotherapy that had been our approach for the treatment of lung cancer for decades. Chemotherapy that prolongs survival, improves quality of life. Here we compared that to immunotherapy, and what we saw from that phase III trial was immunotherapy was better in every conceivable way. Better in terms of response, progression-free survival, the durability of control, and overall survival. Importantly, it's also better in terms of toxicity. Immunotherapy became our standard of care based on this trial for patients whose lung cancer had high expression of a protein called PD-L1. That's about a third of patients. These are updated data looking at five-year survival rates. Let's pause there and acknowledge the importance of that sentence, five-year survival rates. Decades ago, we wouldn't even conceive of anyone surviving five years with a stage 4 lung cancer diagnosis. Here, what you can see is almost a third of patients alive at five years. This study was presented in 2016, and so we have even longer follow-up. On the next slide, we see eight-year survival data. At eight years, we have almost a quarter of patients alive at eight years. Here we see 24% of patients at eight years. Notice that there's not a whole lot of difference between the six-year survival rate and the eight-year survival rate. I think a better mark is how many of those patients have not seen any evidence of progression. If we look at the next slide, while 24% of patients are alive at eight years, we see 13% of patients are progression-free. 13% of patients. In this study, patients received two years of immunotherapy and then are observed, and for 13% of patients enrolled in this trial, six years with no therapy, they have still not seen their cancer come back. The word cure is a tricky word. It's an emotional word and a hard word to define, but are these patients cured? I believe that some, if not all of these patients are cured. We are able to cure some patients, but notice it is the small minority of patients, only 13% of patients, but it is possible. Now, so to speak, we've bitten the apple. This is really the bar. This is what we're capable of, and what we want to do is deliver this to more patients, more than 13%. Also remember that this study was done in patients with high PD-L1 expression, which is about a third of our patients. What about the other two thirds? What about most people with advanced lung cancer? Again, this is only a small subset. If we look at the next slide, we see long-term follow-up from a regimen called KEYNOTE-189, which was immunotherapy with chemotherapy. This regimen looked at standard state-of-the-art chemotherapy, platinum plus pemetrexed, either with placebo or pembrolizumab. What we saw was adding immunotherapy to chemotherapy improved progression-free survival, and importantly improved overall survival. As we saw with the prior trial, it led to a chance of long-term survival. Here, the five-year survival rate, almost 20%, almost one in five alive, and this includes all PD-L1 strata, really an entire all-comer population within a non-squamous histology. On the next slide, how many of those patients are progression-free at five years? It's the minority. It's about 7%-8%. Breaking it down by PD-L1 expression, for PD-L1 high, 13% of patients progression-free at five years. For PD-L1 low, about 7% of patients progression-free. For PD-L1 negative, only 2%. It's a small minority of patients, but what we've seen with immunotherapy strategies and recapitulated across many different immunotherapy agents is long-term survival and long-term progression-free survival is possible. It is not most patients, it is certainly not enough patients, but it is some patients. This is what we're chasing for all patients. All of our patients deserve this opportunity, so immunotherapy remains our standard of care for every non-small cell lung cancer that does not have an actionable target, which is most lung cancer. All patients deserve that opportunity. Most will not achieve this result. What our job is, what our vision, our goal, our hope, our dream is to deliver this to all patients. How do we get there? If we look at the next slide, the overall summary here is that most patients do not respond to immunotherapy. A small subset do achieve durable response, but another subset achieve a transient response. This, I think, intellectually is very intriguing. On the next slide, we see follow-up from that KEYNOTE-189 study, and in dark green you'll see the course of therapy two years with pembrolizumab. If we click ahead to the next slide, in dark green here we see the two-year course of pembrolizumab. What we see with the black dots, those represent progression events. While some patients have progression of their cancer early, some patients do have it late. Some don't have it at all, and that's certainly what we hope for, but some do progress late. These are instances where we feel we're very close to getting that immune response, where we were able to engage our immune system, but not in a durable way. This is really what we want to achieve, more durable immune responses. For patients whose tumors initially responded but lose response, we really want to recapture that response. Because what is our alternative here? For patients who initially receive chemotherapy and immunotherapy and then progress, the current standard of care is docetaxel in the U.S., docetaxel with ramucirumab. This is a tough regimen and the outcomes are poor, but it is a regimen that we have not been able to surpass. When we look at the outcomes with standard docetaxel and ramucirumab, the response rate is 23%, only a fraction. With docetaxel alone, which is the global standard, only 14% of patients will respond. 14%. The progression-free survival with docetaxel alone was three months, which is really the first scan. Any benefit is fairly transient and the survival remains between 9 to 10 months. Outcomes with docetaxel are very poor and the safety leaves a lot to be desired. Patients do not feel well with this treatment. Fatigue is seen in most patients, with 14% having grade 3 or very severe fatigue. Patients do not feel well. Neutropenia, or low white blood cell count, seen in 55% of patients. Most of those, almost all, are grade 3 febrile neutropenia, dangerous complications seen in 16% of patients. About a third of patients require some dose hold or reduction or adjustment in some way. This is a regimen that we do not like prescribing. It has a ceiling on how well it can do. Patients do not feel well with the treatment. We need something better to offer to patients, but we haven't seen anything better for quite some time. We're long overdue for an advance. While we appreciate the advances with immunotherapy, we're ready for something more. To wrap up on the next slide, where we see things currently with non-small cell lung cancer without a driver alteration, immunotherapy is our standard of care, clearly superior to chemotherapy alone, and importantly offers the potential for long-term survival. We celebrate this advance. We offer hope to our patients. For most, the likelihood of long-term survival is quite low. We can celebrate the advance while still acknowledging the unmet need is pressing and looms large. Progress has stalled. While immunotherapy is state-of-the-art, the KEYNOTE-024 was FDA approved in 2016, chemotherapy with immunotherapy in 2018. Almost a decade since some of these have been approved, we still haven't improved upon that. The pursuit of transformative change really lies in finding durable survival. What we do not want, what we do not need, are incremental benefits with cytotoxic molecules. What we want for patients are more immune-mediated anti-tumor responses that have meaningful, durable survival and progression-free survival. This is really what we're chasing, and our hope is that this program will get us closer there. With that, I'm happy to turn things over to the next part. Many thanks, Stephen. Now we'll pass to Benjamin, Institut Gustave Roussy. Sure. Happy to be there. I'm Benjamin Besse. I'm a medical oncologist, mostly thoracic oncologist and Head of Clinical Research at Gustave Roussy. Now we will talk about therapeutic vaccination and Tedopi in patients with non-small cell lung cancer. There are two main kind of vaccines. Those that are ready to use or off-the-shelf, which are vaccine already prepared that can be based on protein, on mRNA, and Tedopi is one of them, with a mixture of neoepitopes, and it's dedicated to patients that have an HLA-A2 positive phenotype. Other vaccine are personalized. Usually they are mRNA vaccines. They are quite costly and difficult to make, with a turnover time that is usually between six and seven weeks because you need a biopsy or surgical specimens of the tumor and then you generate the vaccine, the personalized vaccines. We will talk about Tedopi that is a ready-to-use one, as I said. Next slide. What is Tedopi? It's a combination of neoepitopes. It's nine optimized neoepitopes that will cover roughly 100% of non-small cell lung cancer. You don't have to adapt the vaccine to the expression of the neoepitope. It's ready to use to any kind of non-small cell lung cancer, squamous or non-squamous. There is a binding to HLA-A*02, so we have to restrict the population to HLA-A*02 positive patients, which represent 45% of our patients. It's a ready-to-use emulsion that is given subcut each three weeks. Next slide. The first phase II study was done in 64 patients with non-small cell lung cancer, and all these patients were chemo-pre-treated. The overall survival of the vaccine is quite impressive in this pre-treated population, 17.3 months. It's obviously restricted to HLA-A*02 positive patients. Interestingly, in this sub-analysis, OSE look at the benefit of the vaccine based on the neoepitope response. You measure in the blood the immune response to each of the nine neoepitopes. The more immune response you have against neoepitopes, the better is the survival, which is a strong indication that the activation of the immune system, the specific activation of the immune system by Tedopi, leads to a disease control and a benefit of overall survival. The second point is, you remember all these curves on immunotherapy in first-line that Stephen showed. All these curves, as he highlighted, a plateau. The shape of the curve is really that you have long responders in these patients. Interestingly, even in the patients with a lower neoepitope response, you can see the shape of the curve with low responders. Next slide. These drove to the development of the first phase III trial in patients with non-small cell lung cancer, pre-treated with chemo and immunotherapy. It's the phase III ATALANTE-1 trial. Next slide. The trial was done in second line, as Stephen presented. When you diagnose a non-small cell lung cancer, you have to look at the targets that make the patient eligible for targeted therapy. That will be roughly 15% of the Caucasian population. All the other ones will receive immunotherapy or chemoimmunotherapy. At the time of progression, there is only one standard of care, that is docetaxel, a standard single-agent immunotherapy. Quite toxic, I have to say. Next slide. There have been a lot of attempts to beat docetaxel as a standard of care. A few years ago, we had a lot of expectation with two type of strategy, VEGF-R inhibitors, and this is example of two phase III study that have combined an immunotherapy plus a VEGF-R inhibitor and randomized against docetaxel. The two trials are negative for overall survival, but there are four randomized trial with four different combination of anti-IO plus a VEGF-R inhibitors, and all these studies are negative. The other class of drug that is really under the spotlight is the ADC, the antibody-drug conjugate. These are agent that were given single agent and combined head-to-head with docetaxel second line, again, post chemoimmunotherapy, none of these drugs made it. Even if some of the trial were statistically significant, the clinical benefit was not enough to have an FDA or EMA approval. That now standard of care, even with all this development of new drugs, standard of care is still docetaxel for the second line. Next slide. In the ATALANTE trial, Tedopi was randomized 2: 1 to docetaxel, the standard of care, in exactly this population, which we just described. Patients with advanced or metastatic non-small cell lung cancer with an HLA-A*02 positive test. EGFR mutation and ALK fusions were excluded. Any PD-L1 status could be enrolled. All the patients had to progress under chemoimmunotherapy given sequentially or both combined, but the last line had to be the immune checkpoint blockers. The patients were randomized between Tedopi and docetaxel, and the primary endpoint was overall survival. Next slide. The trial aimed to recruit almost 320 patients, but because of the COVID pandemic and the new vaccine for COVID, the trial was stopped after inclusion of 219 patients. These patients had first or secondary resistance to immunotherapy, meaning that they received less or more than 24 weeks of immunotherapy. The primary population that we define was those patients with secondary resistance. All these patients that receive at least 42 weeks, six months roughly, of immunotherapy, and that represents 118 patients. Next slide. In this primary population, if we compare to the intent-to-treat population, the patients' characteristics are overall quite the same. The percentage of squamous, in particular the TNM stage at study entry, or the rate of brain or liver metastasis. It was roughly similar. Next slide. In the primary population, these patients with secondary resistance to immunotherapy, you can see a significant and clinically significant improvement of the overall survival. 7.5 months in the control arm, what you expect, versus 11.1 months in the Tedopi arm, with a hazard ratio of 0.59. Next slide. If you look at the subgroup where you could see a benefit, the only subgroup where there is zero benefit, apart from the stage 3, but as you can see it's a very small population, difficult to have any conclusion, it's the patients with brain metastasis. In the current trial, these patients are excluded. Next slide. If we look at the time to worsening of the performance status, it was much better in the Tedopi arm compared to docetaxel arm, and it's related to both the efficacy and the toxicity. Next slide. If we look at the toxicity of the docetaxel or Tedopi, it's striking to see that you have three times less severe grade 3 to 5 adverse events with the vaccines compared to docetaxel. In term of toxicity profile, the vaccine is much better in a lot of parameter, hematologic toxicity, but also very important parameters such as alopecia. Docetaxel induce alopecia where a vaccine doesn't. This is also why the quality of life was better in the Tedopi arm compared to the chemotherapy, both because it's more effective and because you have less toxicity. Next slide. As I said, this trial was stopped because of the pandemic and the subgroup analysis of the secondary responder shows strong benefit, but it was not enough to put the drug on the market. It was enough to have a very strong hypothesis to build a new phase III trial in a much more precise population. The patients with non-small cell lung cancer pretreated with chemoimmunotherapy, HLA-A2 positive, and with secondary resistance to checkpoint inhibitors. Next slide. This is the main characteristic of the trial, the population, HLA-A2 metastatic non-small cell lung cancer with secondary resistance to immune checkpoint inhibitor defined by at least 24 weeks of immunotherapy. Docetaxel was accepted by FDA as a standard of care for the comparator arm. The primary endpoint is overall survival. This is really meaningful and convincing for such trial. Among the main secondary endpoint, the patients reported outcome and quality of life was accepted by FDA. There is a central HLA-A2 testing with a companion diagnosis test, and this lead to, next slide, this design. In the ARTEMIA study, an ongoing phase III study, Tedopi is against compared to docetaxel, but in this well-defined population, HLA-A2 positive, squamous and non-squamous non-small cell lung cancer pretreated with chemo and immunotherapy and with secondary resistance, so at least 24 weeks of immune checkpoint inhibitor. As I said, because of the subgroup analysis, the brain mets were excluded. Primary endpoint is overall survival, and there is a stratification on histology, squamous and non-squamous, and performance status. The trial is now ongoing. While I will stop here and give the word to Alex that has presented the results in the ovarian cancer. Many thanks, Benjamin. Up to you, Alexandra. Thank you. I have a first slide. I'm Alexandra Leary. I'm a medical oncologist at Gustave Roussy and Deputy Head of the Department of Medical Oncology, and I'm also the President of the National Intergroup for Clinical Trials in Gyn Onc. Next slide. Before I jump into the trial, because we've talked only about lung cancer so far, I'm just going to give a 30-second introduction on ovarian cancer. Ovarian cancer is not as frequent as lung cancer, but it's deadly as well. 80% are diagnosed at an advanced stage where we do chemo and surgery, and for years, the five-year survival without disease in ovarian cancer was less than 2%. When we're talking about cure rates, even in upfront surgically resected ovarian cancer, our cure rate was 2%. Absolutely horrible prognosis. This has clearly evolved with better surgery and the advent of targeted therapy such as PARP inhibitors and bevacizumab. Actually today, by putting chemo, surgery, and using these maintenance options, we've dramatically improved survival, with now five-year disease-free survival close to 40%, which is great. That's excellent news. For years, when they relapsed, we would do platinum again and platinum again and platinum again. That was our favorite chemo. It worked every time you put it in again. Unfortunately, by doing much better in first line, those who are not cured in first line and progress under the pressure of something like a PARP inhibitor or after bevacizumab, suddenly when we were putting a platinum again, it wasn't working as well. Okay? We have no maintenance strategies for these patients. With that in mind, I'm going to present the result of this randomized, international, academically sponsored trial testing the neoepitope-based vaccine OSE2101 that you've just heard about, plus or minus an anti-PD-1 pembrolizumab versus best supportive care as maintenance in these platinum-sensitive relapse patients with ovarian cancer. Next slide. Again, why we did this study. Actually, platinum-sensitive ovarian cancer used to be easy to treat, and today it's an area of unmet medical need. Okay? We have no approved maintenance strategies for these patients who relapse, who we treat again with six cycle of platinum, who previously received bevacizumab and previously received a PARP inhibitor. No more maintenance. We just have to do watch and wait. The other thing is there hasn't been a single positive randomized trial in this setting for platinum-sensitive relapse ovarian cancer in years, over five years. This is despite huge phase III trials testing immune checkpoint inhibitors as maintenance on their own with bevacizumab, with PARP inhibitors. All negative. As I said, these patients who progress post-PARP have poor response when you reintroduce the platinum. Even if you manage to get some platinum in, we stop it usually after six cycles, they relapse really shortly thereafter. Next slide. I'm not going to give again the background on this vaccine, which has been very well introduced. It's relevant in ovarian cancer because 80%-90% of ovarian tumors express one or more of these tumor-associated antigens. It's important, they're not just tumor-associated antigens. These have been modified to increase their binding capacity to the T cell receptor and/or to HLA-A2. Given the positive results in lung cancer with acquired immune checkpoint resistance and the fact that so far immune checkpoints alone or with PARP or with bev weren't being efficacious in ovarian cancer, we thought we would use this vaccine to turn what is frequently described as an immune cold tumor into an immune hot. Okay. That was the aim of this study, was to evaluate the benefit of combining this vaccine with an anti-PD-1 as maintenance after platinum in this very difficult-to-treat patient population. Next slide. The design was rather simple. Basically, any patient who was relapsing and eligible for platinum doublet received a platinum doublet, four to six cycles, and had at least their disease controlled. Stable disease, partial response or complete response, who had previously had a PARP inhibitor, previously had bev or had a contraindication. Therefore, there's no maintenance options for these patients. If they were HLA-A2 positive, they were randomized to the standard of care, which unfortunately is watch and wait or best supportive care versus the vaccine on its own versus a combination. The randomization was 1: 1: 2. Next slide. Without going too much into the statistics, it was three arms, but we designed the trial with a sample size of 185 patients to have the power to detect an important difference between the combination of the vaccine and pembro versus best supportive care. Okay. Next slide. The patient characteristics I probably won't go into too much for those of you who are not ovarian cancer specialists, but they're as we expect. They were very pretreated with PARP, pretreated with bev. Roughly half of them had stable disease, half of them were in complete or partial response to the chemo when they were randomized. Next slide. These are the primary results. Okay. The combination of vaccine with pembrolizumab as maintenance after platinum significantly decreased the risk of progression by 50% compared to standard of care. The hazard ratio is 0.53 and a highly significant P value. The trial is positive. We achieved the result we were hoping to get. That's for the primary endpoint. Next slide. Although we weren't powered to do this, we couldn't help but look. When you compare the three arms between each other, there's an incremental benefit for the combination compared to the vaccine on its own, and there's an incremental benefit for the vaccine on its own versus best supportive care, although this did not reach statistical significance. Next slide. The safety was actually interesting. The vaccine had been previously tested and very well tolerated, as Benjamin said. We did have more immune-related toxicities in the combination. We know an anti-PD-1 alone, vaccine alone, and we were seeing more immune-related reactions with the combination than we expected, which we actually, while the trial was going on, considered a good sign that we were stimulating the immune system. The most common, grade 1 or 2, were local site injections. Okay? Having seen some of Benjamin's patients, who were men and women, at least in my women-only population, it seems they get more local site reactions. Grade 1 or 2, but they're there. The intriguing one was the cytokine release syndrome. They were very rare with the vaccine alone in previous studies. It was very rare in our vaccine-alone arm here, with 9%, mainly grade 1/2. We were seeing more, mainly grade 1/2, cytokine release syndromes with a combination of vaccine and an immune checkpoint. Okay? Again, at least proving that we were achieving what we wanted to achieve. Therefore, halfway through the study, we said, "Okay, we're going to put just very simple primary prophylaxis with basically paracetamol and non-steroidal anti-inflammatories." With that, we significantly decreased the risk of grade 1/2 CRS. Next slide. When you look at the subgroups, the benefit was seen across the subgroups. If you look at HRD negative all the way at the bottom, it suggests no benefit. There's 13 patients, I think it should. In a multivariate, it was negative and there was no interaction. On multivariate analysis, the only group that appeared to have especially great benefit were the patients who were in partial or complete response to chemotherapy, where there, the hazard ratio was 0.31, which is really quite remarkable. Next slide. In conclusions, we present the first trial providing a proof of concept for the benefit of a vaccine approach in ovarian cancer. This is also the first positive randomized trial in the platinum-sensitive setting ovarian cancer in years. The combination of the vaccine with pembro as maintenance after platinum significantly reduced the risk of progression by 50% and by almost 70% in those in CR PR. There was a little bit more toxicity, but it was mainly grade 1/2 and quite manageable once we introduced really simple prophylaxis. This study, its control arm confirmed that these patients who relapse, they get another platinum. Their prognosis is terrible if they have prior PARP exposure. Once you stop the platinum, their PFS is less than three months. We really feel this supports a phase III confirmatory registration trial. Last slide. Do I have any more? Next one. This was sort of the lay summary. Just a reminder that women with ovarian cancer who receive platinum-based chemotherapy when their cancer comes back after prior bev and PARP have a poor prognosis. Okay? That's on, let's say, the flip coin of the fact that we're doing such great treatment in first-line. Unfortunately, if that doesn't cure them, when they relapse, they're harder to treat. The Tedopi trial showed that giving a combination of an anti-tumor vaccine with immunotherapy as maintenance after platinum significantly delayed cancer progression. As I said, this is the first positive randomized trial in years for this patient population and the first proof of concept. We're really excited about this data, and we can't wait to go to the next step. Thank you very much for your attention. Many thanks, Alexandra. Now we are moving to questions. First I would like to thank, in particular, Valérie Gabard, our Head of MSL, and Thomas Gidoin, our CFO and Deputy CEO, who have prepared this webinar. I think that we have a first question coming from Aaron. Aaron asked the question. I'm not so familiar with that, so maybe I will read the question. When we look at the population of interest for Tedopi's evaluation in non-small cell lung cancer, don't you think that we address Tedopi to a very restrictive population with the double restriction of HLA-A02 phenotype and secondary resistant to checkpoint inhibitors? Benjamin, maybe can you answer this question? Sure. Since more than 20 years now, we are heavily used in non-small cell lung cancer to treat subgroup of patients that are started with EGFR inhibitors and then ALK and then ROS1, and we have now 10 targets that we have to screen in all the patients. Some of these targets, like BRAF mutation, is 1% of our population, and that's enough to develop a randomized trial and to approve drug on the market. In lung, we are very used to screen for markers and treat subgroups. No, we think that this population will represent roughly 15% of the patients that progress after chemoimmunotherapy, which is a huge number for you. I don't see that as a limitation. Thank you for that. Sorry, Stephen. Sorry. Yeah. Echo Benjamin's thoughts here. We're used to dealing with small populations. I'll mention in the U.S., HLA-A*02 is 40%-50% of patients. This is the most common that we would subtype as well. You have to start with where the drug is going to perform best and follow the science, and I think that's the starting point. If this really confirms our suspicions that this is an effective treatment. I think that it opens the door to further modifications, which can expand its use in different indications. The HLA-A*02 is the most common subtype. Thank you so much for that. I think that Aaron is connected. Would you like to ask oral questions, if we can do that technically? I'm not familiar with that. I'm not sure it works like this. Thibault? Hi, can you hear me? Yeah. Excellent. Fantastic. Thank you for the event today, thanks for taking my question. Curious to learn if the ARTEMIA trial results are positive, how quickly do the KOL think that Tedopi could fit into the second-line treatment pathway? What, if any, physician education or diagnostic infrastructure would be needed? I can start with the U.S. answer. Very quickly, again, the endpoint here is overall survival, we are eager for something to replace docetaxel. As Benjamin outlined, there have been many large phase III trials that have simply failed to improve outcomes. If we do demonstrate an OS advantage, I think that there would be a very enormous appetite to move this forward fairly quickly. First on guidelines, then certainly through the FDA process. HLA subtyping is done pretty routinely as part of most of our commercially available next-generation sequencing panels. In the U.S., we often know that information up front, we wouldn't have to have big changes in terms of our current testing practices, at least for most institutions. The timelines would be a little different in Europe, I imagine. Regarding Europe, HLA-A*02 is a very simple blood test, I don't see any issue to have HLA-A*02 as a reflex testing. It's something that is intrinsic to the patient, it's not something that appears with resistance, for example. You can screen up front when the patient is diagnosed or start his first-line chemo IO and when you have a doubt of progression. The testing will be something very easy. As Stephen said, we all want to give something else than docetaxel. I think the uptake of such vaccine would be very massive. Thank you for that. Aaron, do you have additional questions? Yes, thank you very much. One more question from me, perhaps that's for Alexandra. Looking at the ovarian cancer program, the data was really encouraging, so thanks for presenting that. Please, could we hear your thoughts on what a credible subsequent study might look like in terms of design and how it would build on from the prior trial? That's a very good question. It is a matter of discussion because we just got these results. When we designed this trial, the acceptable standard of care, the only available standard of care in this setting was best supportive care. Today, it's becoming increasingly unacceptable not to give any maintenance, okay? Even though we don't have reimbursements, which is a bit of a problem. One idea would be to say, well, there is data to support putting an anti-angiogenic in people who are previously exposed to bevacizumab. And would that be appropriate to add an anti-angiogenic component both in the control and the experimental arm? PARP inhibitors, we don't have any data, but we have a large phase III study that supports bev after bev or anti-angiogenic after anti-angiogenic. That would be one slight modification, which I think ethically and even just it makes sense. Perfect. That's very helpful. Thank you very much. No more questions from me, but look forward to following the progress. Thank you for that. We have written questions. With the rapid emergence of other approaches like ADCs bispecifics, next-gen immunotherapy, where do you see Tedopi fitting into the treatment algorithm in the coming years? Do you view Tedopi primarily as a standalone therapy, or do you believe its greatest potential could be coming from combination strategies with checkpoint inhibitors, ADCs, other immunotherapies? Hello, I may start. When we design ARTEMIA, a lot were thinking that ADC would be the standard of care, and it's not on the phase III or negative. Other strategy also not there. You're talking about bispecific. Genmab had a randomized study with GEN1046, which is a PD-L1 4-1BB bispecific antibody, and they stopped the phase III study. It seems to be not based on data, if I understood correctly, but they stopped the program. LATIFY was also a very promising study with ceralasertib, an ATR inhibitor combined with IO in second-line compared to docetaxel, and the trial is negative. The signal that we have from ATALANTE-1 is quite strong in a situation, in fact, where all the phase III so far fail. I don't see, and maybe Stephen, you have other idea, but I don't see an asset that have, well, let's say much more activity than the one that I just alluded to. No, I don't see in the upcoming years the standard of care changing. Yeah. I think that ADCs have shown a lot of promise, really across tumor types, but at their heart, they are still cytotoxic molecules. While they can offer responses, they still share a lot of toxicities that we see with standard chemotherapy. I think that will be a challenge to a lot of patients, particularly in the later line settings. I think that the difference with Tedopi is it really is an immune-based strategy. It can really make a big difference, both in terms of quality of life and overall survival. These immune-based strategies offer, I think, the potential of much more durability than we might see with something like a cytotoxic agent. ADCs, there are a lot, it's a crowded field. I suspect just by sheer number that one of these studies will be positive. How much of a huge impact it'll make remains to be seen. I still think that there's an appetite for an immune-based strategy. In terms of monotherapy versus combinations, I think once you demonstrate that this offers a survival advantage as monotherapy, you open the door to all sorts of combinations. Whether that's with bispecifics or with checkpoint inhibitors, could that further long-term survival odds and could that really enhance those immune-mediated anti-tumor responses is something that I'm very optimistic for. Of course, first we have to demonstrate clear efficacy as a single agent before we explore combinations. I see no reason why this wouldn't be able to be combined with other strategies. In terms of the ovarian cancer space, I sort of have the same answer. As I said in my introduction, people have tried to get a new standard of care in maintenance platinum sensitive, and they have not managed with immune checkpoint inhibitors on their own, or when they combine them with what we thought was the best, such as PARP inhibitors. It didn't add anything. There's not so much out there. There are ADCs that are being explored everywhere. They're putting them in every indication, and a lot of them as maintenance. Let me tell you, an ADC as maintenance is not the same thing as an immune therapy as maintenance in terms of quality of life. Okay? For now, it'll be a while before we get even the opportunity of a positive study with an ADC in the platinum sensitive setting. We do believe in combining it because we've already combined it with an anti-PD-1, and I think it might be worth thinking about combining it with an anti-VEGF. I think it's nice to have a maintenance that doesn't have a cytotoxic in it. Thank you for that. An additional question regarding TEDOVA. Did patients presenting CRS benefit better from the treatment from Tedopi than others? It's an excellent question. No, we couldn't see that. One of the reasons is that in the early part of the trial, we didn't expect CRS. Gyn oncs haven't done a lot of CAR T-cell therapies and TCR modified T cells. When they saw CRSs, a lot of the investigators were a little shocked, and actually, my concern was they were going to stop the treatment. That's why I introduced the prophylaxis. Okay? However, when we look at prophylaxis, people who came in sort of in the effective phase and had prophylaxis, they seemed to benefit more, probably because those patients with CRS probably are good candidates. Once we had the prophylaxis, they had very low-grade CRS and they continued. Okay? It's sort of a sweet balance between causing an immune reaction, but we don't want it to be scary enough that the investigator or the patient says, "I don't want anymore." I think by introducing the prophylaxis, we helped with that. Okay. Very clear. Thank you for that. Another question regarding Tedopi, TEDOVA, sorry. You mentioned a poor prognosis, Alexandra, what is the, in your, let's say globally, the current median overall survival and what would be something that you would define as clinically relevant, assuming that you will get this data, I don't know, probably later this year or next year. What would be the median overall survival improvement, let's say, clinically relevant for you? Demonstrating improvements in overall survival in ovarian cancer in clinical trials has been challenging. Okay? Finally, we've arrived there for the first time in, I think, three decades, a couple of weeks ago in the resistant setting. Okay? The resistant setting is not where I am here. It's patients, they've become resistant to platinum, and here the standard chemotherapy doesn't work. It's a little bit like the docetaxel, right? They don't have subsequent lines of therapy. If you have a PFS benefit in that setting, it is easier to translate into OS. Finally, we have two positive clinical trials in the resistant setting that showed an OS benefit. All of our studies in first-line or subsequent sensitive setting, we haven't been able to translate PFS benefit and OS benefit because subsequent therapies still work. Now, again, this might change because here in the post-PARP setting, that might change. I don't like to talk about numerical benefit. Here we have a hazard ratio of 0.53 of PFS. If we get a hazard ratio that's positive, 0.7, 0.8, no one has ever achieved that in first-line or platinum-sensitive relapse. Any impact on OS, to me, would be a great success. Very clear. More sophisticated question. I'm sorry, I will try to read that carefully. Given that Tedopi targets multiple specific antigens to turn cold tumors hot, have the translational data from TEDOVA shown any evidence of epitope spreading to non-targeted antigens? The work is ongoing. We have collected PBMCs. We're working with an academic lab to do all of this. I haven't yet seen the data, so I'm not hiding anything from you. We'll be very interested to see some of the data that was already generated by Benjamin in the previous long trial suggests that the epitope-specific response might be relevant. As to the rest, I don't yet know, but we have a very comprehensive translational program, as well as targets and the expression in the tumors themselves, detect P53 mutations. We have two types. One is the loss, and the other one is overexpression. That's probably relevant. There's a lot of work still to be done, and we look forward to presenting that in subsequent presentations and publications. Fantastic. Thank you so much. I think we're coming to the end of this webinar. Thank you so much to the three of you for all your dedication to patients first and to science globally. We're very, very enthusiastic at OSE to move forward with Tedopi, of course, in non-small cell lung cancer in the very short term, and assuming that we have financial capacities in ovarian cancer and maybe in other indications. I thank you so much, and I thank all the participants to this webinar. It is recorded, so this will be available probably for the next few weeks on our website. I wish you a great day and talk to you soon. Thank you again.