Hello, everyone. I am Marc Le Bozec, CEO for OSE. We are here today to talk about Tedopi, our immunotherapy, which is in a registrational phase III for non-small cell lung cancer. Most recently, we had the pleasure to see a presentation by Professor Federico Cappuzzo at ESMO on October 25th, for an additional clinical trial, which is called Combi-TED, that will be explained further in this presentation. We also have the pleasure to have Professor Stephen Liu of Georgetown University, who will give a broader view on the way non-small cell lung cancer is addressed. In few words, I would like to introduce you to our company. OSE is a company that has been listed on Paris Stock Market since 2015. We have two lead compounds. One is lusvertikimab, an anti-IL-7 receptor monoclonal antibody that has delivered positive phase II data in ulcerative colitis last year.
We are preparing a subcutaneous formulation that should be available mid-2027. On top of that, we are preparing a new clinical trial on the narrower indication with our IV material, which is called chronic pouchitis, which is a subset of ulcerative colitis. We have, of course, Tedopi, which is the star today of this webinar. This is an immunotherapy, a combination of 10 neoepitopes that have been given to more than 800 patients so far in various clinical trials. In particular, in the most recent trial that has been presented at ESMO once again, which is called Combi-TED. You can see here that Tedopi has been tested in various clinical trials with success. Currently, once again, we are in a registrational phase III. Our target is 363 patients, and we are coming close to this number. We are very proud of that.
I will not spend too much time introducing the company. I think what is of the essence is to listen to Professor Cappuzzo and Professor Liu, who will give you a broader vision and a real-life experience of our compound, Tedopi. I pass now to Professor Liu of Georgetown University.
Great. Thank you for having me and the opportunity to set a little bit of background for the potential role Tedopi could place. I would like now to go over a few slides on the unmet need in non-small cell lung cancer. As we are aware, we have undergone transformational change in the management of this disease. If we look at the next slide, we can see a little bit of the demographics and some of the numbers of lung cancer. These are numbers for the U.S. projected in 2026. As you can see, lung cancer, highlighted by the arrows, will be the second most common cancer for both men and women, behind prostate cancer and breast cancer. Incidence numbers, and on the next slide, I am showing mortality numbers.
And while it is the second most common, it is by far the most lethal for both men and women, surmounting the next few combined. It is the most lethal cancer in the U.S. and has been for quite some time. If we look at the next slide, just for reference, we can see our five-year survival numbers. While breast cancer is the most common for women, prostate the most common for men, we have five-year survival rates north of 90%. We have made remarkable advances. We are very proud of that as a community. We see a big drop-off in colon cancer, where our five-year survival rates are now down to 65%. When you look at lung cancer, the five-year survival rates are even lower at 28%. 28% is the best we have ever had by far, and yet you can see how it pales in comparison.
I think this really speaks massive need for newer lung cancer treatments. How do we treat lung cancer? On the next slide, really, we think of two general categories. While chemotherapy can play a role, we are looking at two major paradigms, one of targeted therapy. This is for molecularly defined subtypes of lung cancer, such as those harboring mutations in EGFR or fusions in ALK. For those where we have a match, we deliver targeted therapy. Very high response rates, low toxicity. These are not cures. For most patients and most targets, we expect resistance within one or two years. The other type of treatment we are employing really is immunotherapy, harnessing the power of our own immune system. This is appropriate for most lung cancers today. It can be given as monotherapy or in combination with chemotherapy or other immunomodulatory agents.
We have a long track record with this. On the next slide, we show the results from KEYNOTE-024. This really started our paradigm with frontline immunotherapy, revolutionary trial, looking at the PD-1 inhibitor pembrolizumab, comparing it to standard chemotherapy. Pembrolizumab superior in every way for patients whose tumor expressed PD-L1 at a high level. It is about a third of patients. We can see pembrolizumab had superior response rate, progression-free survival, improved safety profile, and much better long-term survival. When we look at the survival benefit, this is despite allowing crossover, despite having immunotherapy freely available, we see the clear survival benefit with immunotherapy cementing this as our preferred option. We now have longer follow-up. If we look on the next slide, these are eight-year outcomes. The eight-year survival rate at 24%, something we had not dreamed of before. Metastatic lung cancer, one in four alive at eight years.
This is transformation. But you can see it is the minority. Some of these patients are cured, but not most. On the next slide, we show progression-free survival. We see our five-year progression-free survival translates to our eight-year progression-free survival of about 13%. So we can achieve long-term survival. I believe we can cure some patients with immunotherapy, but it is not most patients. It is a small minority of patients. This is only for PD-L1 high. A more commonly used regimen, at least in the U.S., is combining immunotherapy with chemotherapy. In the most popular regimen, we have KEYNOTE-189 regimen. On the next slide, we see the overall survival rates with longer follow-up, combining platinum, pemetrexed, and pembrolizumab. We have five-year survival rates just under 20%, a remarkable achievement, one we celebrate all the time. But on the next slide, we see progression-free survival.
That number is quite a bit lower, 7.5%. Can we cure somebody with a stage four lung cancer using chemotherapy and immunotherapy? I think the answer is yes, but not likely, certainly not expected. This is really our goal. This is for non-squamous. On the next slide, we see for squamous, using the KEYNOTE-407 regimen, again, our five-year survival rate's right around 10%. Five-year progression-free survival, rather. Cure possible, but not likely. This is clearly what we want. On the next slide, most patients do not respond to immunotherapy. The transformative nature of immunotherapy is the potential for durability. Not that it works for everyone, it doesn't, but if it does work, it's the one modality we have that could work indefinitely. It's really the quality of these responses. A small subset achieve that durable response. What's interesting is that another subset achieves a transient response.
On the next slide, what we see is a swimmer's plot. These are patients enrolled on pembrolizumab with chemotherapy. In dark green is the two-year course of pembrolizumab. You can see that while some patients do progress early, others, with progression denoted by this black circle, others progress later. Very interesting. We mount an initial immune response, but then lose it. Our immune system was able to control cancer for a period of time, but then we lose control. That's an interesting subset. How can we regain control? These are really different types of cancers. Those that respond to immunotherapy and never stop responding, those that never respond to immunotherapy, where we have more intrinsic barriers to overcome, but that middle group, those that initially respond but then lose it. That's where we think we have a real hope to rekindle an immune response.
What happens when patients do progress? Unfortunately, outcomes and the options remain fairly limited. On the next slide, we show a recent phase III trial looking at a control arm. TROPION-Lung01 looked at an antibody drug conjugate targeting TROP2 called datopotamab deruxtecan. But really, I want to focus on the control arm here of docetaxel, which remains our global standard today. With docetaxel in the second-line setting, and these are phase III trial conditions, perfect conditions, not real-world conditions, we see in this setting progression-free survival of three and a half months with a median survival of less than a year. These numbers haven't moved much. This is still our standard. In addition, while the outcomes are quite poor, it still also comes at a notable cost. Docetaxel, not the easiest drug to deliver. When we look at the next slide at toxicity with docetaxel, it's quite significant.
The rate of dose reduction here, 30%. The rate of interruption and discontinuation, 12%. If we look on the right here, we see high rates of stomatitis, nausea, diarrhea, anemia, neutropenia. The grade 3 and higher rate of neutropenia, 23%. These are patients that have been through quite a lot of treatment. Standard treatment is docetaxel. At relapse, docetaxel not very effective and not particularly well tolerated. Clearly, there's a pressing need for something better, for something more. I'll summarize on the next slide. Immunotherapy remains our frontline standard of care, clearly superior to chemotherapy with the potential for long-term survival. That's why everyone deserves an opportunity for an immunotherapy benefit. But for most subsets, that likelihood of long-term survival is low, and progress has stalled. It has been a decade since KEYNOTE-024. We are overdue for an upgrade and new way to deliver immune responses.
Make it clear, our goal is the pursuit of transformative change, not incremental benefit, not temporizing the situation with cytotoxics or ADCs. What we really want is durable survival. That's our unmet need, a long-term immune-mediated response. How can we get there? There's a lot of excitement on the next slide on therapeutic cancer vaccines. These can come in the form of neoepitope cancer vaccines, which are really off the shelf, widely accessible, or a neoantigen cancer vaccine, which is a more personalized vaccine. Really, I do feel there's room for both. On the left, an agent like Tedopi ready to use, administering to a patient with metastatic disease, stage four cancer, which is the most common stage. On the right, a personalized custom vaccine makes a lot of sense in the adjuvant setting.
We saw recently at ESMO just a few weeks ago, the astounding results of personalized vaccine in the adjuvant setting for melanoma. I think that approach in lung cancer is very promising. But for metastatic, which again is the most common stage, therapeutic vaccines can play an important role. This is where Tedopi can come into play. On the next slide, a cartoon outlining really how these agents work. Tedopi will be delivered by a subcutaneous injection, and then the OSE2101 or Tedopi vaccine's epitopes will be captured in the immune system by antigen-presenting cells, like dendritic cells. These APCs then present those captured vaccines to our own lymphocytes, our T cells, which allows priming and activation, inducing cytotoxic T lymphocytes, clones targeting one of those epitopes.
We then have clonal expansion shown on the bottom right, and this maturation of these T cells will then allow cytotoxic T cells to exert a direct anti-tumor effect. Shown in a little more detail on the next cartoon, on the left here, we see different antigens that Tedopi is targeting. We go to the next slide, we can see MAGE-2, MAGE-3, CEA, p53, and HER-2. These are the epitopes that are being presented to our APCs. On the next slide, we can see some promising results from a phase II study of Tedopi. An interesting premise here. If we have a response to at least three of those five epitopes, we have pretty impressive survival rates. And 85% of patients responded to at least two of those epitopes. So we really do feel we found the right mix here.
On the next slide, this was validated by the prospective phase III ATALANTE-1 trial. This was a trial comparing Tedopi, or OSE2101, to standard of care treatment, either docetaxel or pemetrexed. A bit of an older study where the standard of care in the frontline has since changed. These were stratified by line of prior immunotherapy with a primary endpoint of survival. On the next slide, we can see in patients who had a secondary resistance and acquired resistance to immunotherapy, we see a pretty significant improvement in survival, 7.5 with the standard of care, versus 11.1 with the vaccine, and a much more favorable toxicity profile. That's known as hazard ratio of 0.59. As we know, the frontline standard of care has changed from then to now. This study was curtailed due to the COVID-19 pandemic, and underpowered for the overall analysis, warranting a larger study.
But if we look a little more closely at the ATALANTE-1 study, while there was a survival benefit in those with secondary resistance, on the next slide, we can also see a much better safety profile, as you would expect, compared to chemotherapy. When we look at the related grade 3 to 5 adverse events, 11% with Tedopi versus 35% with chemotherapy. In addition, improvements in quality of life, a positive net treatment benefit versus chemotherapy. Improved survival, better safety profile, quality of life. These are the metrics that we want in a second-line treatment.
So I'll close with the next slide, where we can really put this to test, and that's the ARTEMIA study, a phase III trial that is ongoing now for patients with HLA-A2 positive subtype, including both squamous and non-squamous non-small cell lung cancer in second-line treatment after frontline chemo-IO, with secondary resistance, meaning initial response to immunotherapy defined below, good performance status, stratified by histology performance status in the 2-to-1 randomization to Tedopi, OSE2101, the therapeutic cancer vaccine, versus standard docetaxel. Again, the primary endpoint is the endpoint that matters most, overall survival. Our hope is that this leads to some practice changes and better options for our patients. Thanks so much.
Thank you so much, Professor Liu. Now we pass to Professor Cappuzzo, who will present Combi-TED, the trial he was the principal investigator of. Professor Cappuzzo.
Thank you. Thank you very much for the invitation. I was really excited during the ESMO meeting for presenting this data. If I can have the slides, please. So we go to the first one. Next slide. So what is the rationale for conducting this clinical trial? So we know that in the second-line setting, unfortunately, we have very few options for our patients. Docetaxel is the only agent available in clinical practice. Results are not really exciting. Efficacy is limited. The toxicity represents an important limitation. And we know that the Tedopi is a new anti-cancer vaccine, and it is able to stimulate the immune system, particularly the T lymphocyte, in patients HLA-A2 positive. And we know that because we have clinical results already. Dr. Liu presented some of this data showing that in third line, the Tedopi is effective after sequential chemo-IO failure. Next slide, please.
Based on this data, we decided to design this clinical trial. The Combi-TED was a phase II non-comparative randomized trial in which patients with non-small cell lung cancer relapsing after at least four cycles of first-line chemoimmunotherapy, HLA-A2 positive without mutation in EGFR and without rearrangement in ALK and ROS1 gene, were randomized to docetaxel in combination with Tedopi or nivolumab in combination again with Tedopi, or the control arm was docetaxel. From the statistical point of view, this clinical trial was designed assuming that a 40% rate of one-year survival was enough for considering active this regimen, and therefore, that the regimen needed additional evaluation. If the primary endpoint was met, we also decided to conduct a Bayesian analysis in order to understand the probability that the experimental arms could be superior to the standard arm. Next slide.
In total, we randomized 106 patients, and the clinical characteristics of patients were very well balanced between the three arms, with the only exception that we have more male patient in the docetaxel arm, and we have more never-smoking patients in the docetaxel plus Tedopi arm. The vast majority of patients were PD-L1 positive, approximately 55%-60% of patients. Next slide. The trial met the primary endpoint. The one-year survival rate was 47% for those patients that were assigned to docetaxel plus Tedopi, 46% for patients receiving nivolumab plus Tedopi, and only 29% for those patients receiving docetaxel. The Bayesian analysis also showed that the probability that docetaxel Tedopi arm is superior to docetaxel is 94%, and the probability that the nivolumab Tedopi arm is superior to docetaxel is 92%. Next slide.
In terms of median overall survival, you can see that patients receiving Tedopi had a median survival that was longer compared to patients assigned to docetaxel. The median overall survival was 11.9 months for Tedopi plus docetaxel, 11.3 months for nivolumab plus Tedopi, and only 6.4 months for patients receiving docetaxel. Next slide. For a secondary endpoint, response rate and progression-free survival, progression-free survival was numerically longer for patients receiving the combination of docetaxel and Tedopi, and also the response rate was double for patients receiving docetaxel plus Tedopi compared to docetaxel alone, 20% versus 10%, even if the numbers are relatively small. Next slide. In this clinical trial, no unexpected toxicity was observed. You can see that treatment-related adverse event leading to treatment modification was numerically higher in patients assigned to the two arms, including docetaxel. The addition of docetaxel was responsible for the increased toxicity.
When we look specifically, next slide, to the adverse events that were observed in this clinical trial, asthenia, fatigue, diarrhea, anemia were more frequently observed again in patients receiving the docetaxel. The majority of toxicity was related to chemotherapy. Next slide. These are the conclusion we presented during the ESMO. The Combi-TED trial is a positive trial by showing a one-year survival rate for patients receiving Tedopi together with docetaxel or nivolumab exceeding 40% without any increasement in terms of toxicity. Of course, these data support further evaluation of this compound, and we know that there is the ARTEMIA trial that is currently evaluating the efficacy of Tedopi versus docetaxel in patients with secondary resistance to immunotherapy.
And the next slide is just the acknowledgment for all investigators, patients, families, of course, supporting this clinical trial that was sponsored by our foundation, that is Fondazione Ricerca Traslazionale, with the contribution of OSE and Bristol-Myers Squibb giving the drug nivolumab. Thank you.
Thank you so much, Professor Cappuzzo. We have a first question, which is, can we say that the Combi-TED study is a positive one, assuming that it was not designed to demonstrate superiority over docetaxel?
Yes, this is a positive trial because it was designed specifically to address a question, and the question that we had in our clinical trial was positive. Our assumption was that 40% one-year survival was enough for defining effective the treatment, and we have 47% and 46% survival at one year. So the trial is positive, even if there is no formal comparison with docetaxel.
Thank you for that. We are waiting for additional questions, but I think that everybody is comfortable with the way to ask questions, so if needed, we will re-explain how to do that. There is a new question. Docetaxel is restricted to six cycles, when usually in all studies, docetaxel can be administered until toxicity. When in arm B here in Combi-TED, Tedopi and nivolumab until toxicity. Why this was designed that way, or this occurred that way, Federico?
Well, again, using chemotherapy, particularly docetaxel, for more than six cycles is not. Even if clinical trial indicates this possibility, in clinical practice, it is really difficult that the patient receive docetaxel for more than six cycles, simply because patients progress very quickly. This is the main reason. For those patients not progressing, toxicity is a problem. When we look at the median duration of a treatment across clinical trial, generally it is around four. So six cycles is absolutely enough for addressing the efficacy of docetaxel, for not underestimating the efficacy of docetaxel. In addition, the primary endpoint was overall survival. There is no evidence that by continuing docetaxel for a long time, we really increase the overall survival. Maybe we can have some positive effect in terms of progression-free survival, but not certain in terms of overall survival.
Thank you so much. It is very clear. Now we have a question by telephone by Arron Aatkar from Edison Group. Arron?
The next question comes from Arron Aatkar from Edison Group. Please go ahead.
Hi there. Thank you so much for the presentation, and thanks for taking my questions. First of all, I wanted to ask, given that we have seen encouraging signals now emerging across lung in multiple settings, as well as some other sort of cancer indications, what sort of confidence does that give you in the broader applicability in Tedopi's mechanism across both multiple tumor types and across potentially different settings within lung cancer as well?
Maybe Silvia, you want to answer this question?
So if I understand correctly, the question is that the product, that Tedopi could work across different tumor indications. In fact, for us today, the priority is absolutely non-small cell lung cancer, where in fact we have the ARTEMIA trial, which is again our pivotal registrational study, and it is our absolute priority. We need to be successful there. We are, of course, contemplating additional types of developments, but this will be after the ARTEMIA results, in fact.
Maybe, Stephen, can you add your view on where you would imagine to have Tedopi in the landscape of treating patients that you see on a daily basis?
Yeah, I think there has always been a lot of enthusiasm for vaccines. The science and the logic is so clear, it is so sound. Vaccines should work. They just have not. We can go back to multiple large phase III trials where we really have not seen the signal that we thought we should. I think the ATALANTE changed that, and we took notice of that. Really, it is a matter of finding the right epitopes, presenting them in the right way. But we are ready. There is large appetite for immune-mediated responses. We really want durability. When we look at some of the newer agents, while we are very excited about antibody-drug conjugates, about new targeted agents, these are transient benefits, and they are no substitute for the durability that an immune-mediated response can generate.
Seeing, as you mentioned, a lot of the success in other tumor types, I think it's reinvigorated the optimism for real therapeutic vaccines, and I think the time is right for those in lung cancer. I think the immediate impact would be in the metastatic setting, but certainly every line, every setting could be seen. While the focus here is on HLA-A2, I certainly think that if these show what we think they'll show, this could easily be adapted to other-
Thank you for that. We have another question, I think by telephone from Nicolas Pauillac of Kepler Cheuvreux.
The next question comes from Nicolas Pauillac from Kepler Cheuvreux. Please go ahead.
Hi, guys. Hopefully you can hear me. Maybe just a quick question on my end. I was just looking at the CEMITED data, and inside of that, it looked like you had a very, let's say, low median survival for the docetaxel arm in the study. I mean, it was like 6.4 months. If you compare that to, for example, the data you showed during the presentation on TROPION, that was closer to 11 months. Would you say that there was any driver that would kind of explain the underperformance of the docetaxel in the study? Then the kind of follow-up question on that is there anything to read as to why you were not able to reach the Bayesian threshold you had in the study?
The second question is kind of moving and trying to make some read across into the ARTEMIA study that I guess should result next year. I think there was a delay in the futility analysis. It was kind of linked to delays in the death rate, the event rate. If we think about this study then, should we assume that we will get closer to the usual median survival that we get with docetaxel, and so not make too much read, let us say, from that? Thank you.
Thank you for those questions, Nicolas. So, maybe Federico, can you answer the, let us say, the first part regarding, let us say-
Yeah
the lower performance of docetaxel, as Nicolas said.
I am very happy that Stephen Liu presented also data from the ATALANTE trial, because our data are replicating exactly the ATALANTE trial. So we have a very similar overall survival, median overall survival for both arms, for Tedopi, 11 months, and for docetaxel, that was seven months in the ATALANTE trial. Saying that, we need to consider the type of trial we did, because this is an investigator-initiated trial, meaning that this trial is really close on what happened in clinical practice. Many patients probably were included with clinical condition probably suboptimal. I can say that because we had some early death during the trial in both arms. So probably some patient This is what happened normally in the hospital in clinical practice.
That is the reason why probably the median was a little bit affected in this trial, simply because we are reflecting what happened in a real world.
Many thanks for that. Silvia, can you elaborate on the potential read-across for ARTEMIA?
Yeah. If I may, there was also the question on the 95% with the Bayesian.
Oh, yeah. You are right. Sorry about that.
the Bayesian approach. In fact, as Federico said, it's important to distinguish between the primary statistical objective of the study and the exploratory Bayesian analysis. Primary objective was successfully achieved in both experimental arm with one-year overall survival. The Bayesian analysis was a complementary decision support tool, with a particularly stringent 95% threshold selected to classify the combination as promising. The results, 94.6%, 92.8%, did not formally exceed the threshold, but they provided a very good quantitative assessment of the likelihood, the chance that each combination offers a benefit above the control arm. For us, these results are very interesting for thinking about future development. It's a decision-making suggestions that we got. Concerning the ARTEMIA study, which was right, the other question, and the fact that we have a delay in the futility. This was the question, right?
Yes, exactly.
In fact, we were planning for a futility analysis around August, September, earlier this year. The fact that we are delayed with that, now we plan that around January, February could be the date for that, could mean many things. It could mean that we have two products which work well. Why not? This could be the case. Or it could be that maybe we are a bit delayed with the recruitment, just a couple of months, that could also impact the time for the futility, or the fact that we have a population with a certain good prognosis without brain mets, for example, performance status zero or one. It is too early now, and we need to wait that we achieve the number of deaths that are required for the futility analysis.
Our statistical hypothesis was nine months in the docetaxel arm versus 12 or more for Tedopi. In fact, due to the characteristic, the AGP, the criteria, we think that we will have more patients with the squamous subtype, and with, therefore, a worse prognosis. This is why we selected the nine months. We have to wait in fact.
Thank you for that, Silvia. Even though, of course, as a private company or in public, in this context, as a company, we would like to have a superior effect than what we anticipated of Tedopi. Another question is, why does the curve for Tedopi plus docetaxel goes down sharply after 18 months below the two arms? What is your analysis, Federico, on this?
Well, this is, of course, something indicating the long-term effect of the treatment. For docetaxel, of course, this is not unexpected, maybe this is something that we need to consider, the long-term effect. But here, we are talking about specifically second-line therapy, a setting in which stimulating the immune system, hoping, of course, in a long-term benefit, probably is not the optimal setting.
Thank you for that. Another very precise question is, docetaxel was dosed at 75 mg alone versus 60 mg when combined with Tedopi. What was the rationale for that?
Simply for reducing toxicity. Honestly, I don't think that 15 mg play any role in the efficacy of the compound. Also, we need to consider that the 60 mg/m² is the standard dose for Asiatic patients.
Sure. Thank you for that. In the same perspective, why do we see a quick decrease after six months in PFS for Tedopi plus docetaxel?
For the same reason I already said. The population that was included in this trial was really close to the clinical practice. A part of these patients got a benefit, while for some patients, the efficacy was limited. This is something emerging in any clinical trial with immunotherapy.
Thank you. Very clear. We see that neither arm reached the predefined 95% threshold. Should it be considered as a negative result? I think that Silvia already partially answered that.
Exactly. Yeah.
We are extremely close to the 95%, but I understand that this is a question of statistics. Silvia, you can say a few words about that.
I think that the fact that we are very close to the 95% is very good in any case, and that the 95% is very stringent. It was selected to increase the chances of a success going directly into phase III study, and we are very close to that. The probability, the chance that the experimental arms are better than the comparator, the docetaxel, are still very high. It is a decision tool that we will have to decide whether to follow or not, but the data are very good, and the primary endpoint was positive, was achieved.
If I can add also a comment on that. In any case, that was not the endpoint of the study.
Exactly.
We cannot judge the result if the trial is positive or negative based on this parameter, because that was not an endpoint.
Thank you. Thank you. Very clear. We have a question regarding CEMITED, which is already recruiting. What is the rationale of this study, which is combining Tedopi in first-line maintenance with chemotherapy? What added benefit do you hope, Federico, earlier use of Tedopi will provide?
Well, in my opinion, this is a really logical approach because I think that all these data are going in this direction. Immunotherapy is much more effective when used early during the disease, the story of the disease. So in a maintenance setting, we don't have any interference with chemotherapy or excess in toxicity, and we select also the group of patients not with primary resistance to immunotherapy. That is the population that we know are probably less sensitive even to Tedopi.
Very clear. Maybe a question for Stephen, even it's related to CEMITED. Noticing the plateau in the arm B, like Tedopi plus nivo, could this suggest that Tedopi, in your sense, is restoring sensitivity to PD-1 blockade?
Yeah, I think that's an intriguing possibility. When we think of the functional half-life of PD-1 and PD-L1 inhibitors, quite long, for some people, maybe permanent, which is why we can see long-lasting toxicity in some cases. So it certainly stands to reason that if we're priming T cells with a vaccine, that might have been the missing piece. But I also actually think that plateau sort of contributes to what Professor Cappuzzo had mentioned with the frontline regimen. I think that makes a lot of sense. I think the checkpoint inhibitors plus vaccine are a very natural fit if we can prime our T cells with a vaccine while relieving the checkpoint blockade. I think that allowing vaccines to be given earlier can potentially change some of the cold tumors to hot tumors and evoke more initial responses.
When we think of the role vaccines play in interferon gamma release as well, that combination up front might be able to address both primary and secondary resistance. It's pretty intriguing. Looking forward to seeing those results.
Thank you so much. I think that we are close to the end of the questions. I wanted to thank the teams who prepared this webinar and contributed to all these studies. In particular, I would like to thank Valérie Gabarre, who's been instrumental in putting that in place. I have something to share with you because we're talking on a daily basis with the financial community, in particular in the U.S. We see a strong resistance to cancer vaccines that we can understand after a series of failures. But it's difficult for us to reconciliate your enthusiasm.
I had a chance to meet Stephen and Federico this year several times, and I understand that you have a genuine enthusiasm for Tedopi, and the reluctance, resistance even, of the financial community, it's complicated because we understand that there is a real need for patients, and as physicians, as oncologists, you need new tools to bring some relief to patients, to save some patients. And with this gap, it's for the moment very difficult to understand. Maybe having additional data and explaining again and again the potential of this class of drugs, but in particular, not necessarily the class of drugs, but Tedopi itself, because we have seen many trials, positive readouts in ovarian cancer presented at ASCO earlier this year. CEMITED at ESMO this year, and we're waiting now for ARTEMIA, our registrational phase III. Once again, it's a registrational phase III.
It's not just an additional phase III. But yes, maybe a few words as a conclusion, Federico and Stephen, about your vision as a potential drug in the arsenal, once again, for Tedopi in the coming years. Federico?
No, no, I was really enthusiastic when running the trial, and now we are enthusiastic really for the new study that we are doing. I really hope that we can contribute for increasing survival of our patients. This is what, of course, we want, what we are trying to do in our daily clinical practice.
Thank you for that. Stephen?
I will echo that. I think that when we look at the ATALANTE study, it is quite remarkable that this therapeutic vaccine led to survival gains over docetaxel. The drug works. I think it is a matter of finding the right population and delivering it in the right way. But it is an effective agent that can really prolong survival for patients. So I think that there is a lot of enthusiasm. Vaccines are rooted in science. I think this approach is deeply mechanistic, and I am excited to really see the final results.
Thank you. Thank you very much for participating.