Good afternoon and welcome, everyone. Thank you for joining today's Innate KOL call on lacutamab, where we look forward to sharing updates from data presented at ASH here in San Diego over the weekend. Today's presentation is available on the IR section of the website. On slide two, before we start, I would like to remind you that we'll be making forward-looking statements regarding the financial outlook in addition to product development. These statements are subject to risks and uncertainties that may cause actual results to differ from those forecasted. On slide three, on today's call, we will be joined by Dr. Sonia Quaratino, our Chief Medical Officer, and we'd also like to thank Dr. Pierluigi Porcu, Director, Division of Hematologic Malignancies and Hematopoietic Stem Cell Transplantation, Sidney Kimmel Cancer Center, Jefferson Health, Philadelphia, as our KOL on the call today. Slide four, just quickly to cover the agenda. Firstly, we'll hand over to Sonia for an introduction. Dr. Porcu will then go through the results presented here at ASH from the phase 2 TELLOMAK study before handing back to Sonia for a close, and we'll then open the lines for Q&A. Sonia, I'll now hand over to you. Thank you, Henry. Good morning, good afternoon to everyone, and thank you for joining us on this call. Slide five is a reminder of our strategy. As an early clinical stage company, our business model center around three key priorities, where we look to drive value from our early R&D efforts through later stage partnership, where and when it makes sense to do so. Our ambition is to develop innovative drug candidates that contribute to transform cancer care through a strong pipeline of differentiated antibodies. Firstly, we look to create a near value driven by our lead proprietary product candidate, lacutamab, which is in development for T-cell lymphoma, with updates at ASH, including final Sézary syndrome and early PTCL data. As a reminder, our focus remain to leverage the value of our products as much as possible, which will further validate our science and offer capital that we can reinvest to advance our early R&D engine. We are actively looking to advance the future development, registration, and launch of the asset via partnership, as we have done in the past for other partner assets. Second, we continue to fuel our pipeline and create longer-term value by leveraging our antibody engineering capabilities to develop innovative molecules with a primary focus on ANKET, our multispecific NK cell engager proprietary platform. And we're pleased to see continued progress, with Sanofi presenting various updates for the lead ANKET program, SAR443579, this year at ASCO, ESMO, and also today, this week at the ASH meeting. We also look to move our lead property, ANKET IPH6501, towards phase 1 trial. As we develop antibody targets for our ANKET platform, we recognize some of these binders may be more suitable for ADC therapeutic, and we have announced some further updates in our ADC pipeline last quarter. Last but not least, we are building a strong and sustainable foundation for our business with various partnership across industry and academia. And here, our AstraZeneca partnership with monalizumab is progressing in lung cancer. On slide 6 is a summary of our pipeline, which shows how we continue to translate our science into a robust portfolio of proprietary and partnered assets. It also illustrates how we are executing against our strategy with our lead proprietary assets, lacutamab, ANKET, and emerging ADC, supported by partnered product with AstraZeneca, Sanofi, Takeda, from late to early stage development. We anticipate a series of potential clinical data readouts and catalysts in the upcoming couple of years as our R&D engine looks to leverage our scientific know-how to create a sustainable business. On slide seven, we would like to highlight the presence we have at this year's ASH annual meeting. As well as TELLOMAK phase 2 data, which was presented as an oral presentation on Saturday, which Dr. Porcu is about to cover, we also will update you on some initial phase 1b PTCL preclinical combination and clinical safety data, which was presented on Sunday as a poster presentation. We were also pleased to see our partner, Sanofi, presenting an update on our lead ANKET program, SAR443579, a CD123-target NK cell engager on Sunday. In the presentation, we were encouraged to see further single agent activity and safety for the program in relapsed refractory AML patient. Additional CR, complete response, were observed, with now 5 CR out of 15 patients treated at 1 milligram per kilogram dose level. SAR443579 was well tolerated at doses up to 6 milligram per kilogram, with no dose-limiting toxicities and only 2 grade 1 CRS observed out of 43 patients... The FDA awarded the program Fast Track designation for the treatment of acute myeloid leukemia in May, and we look forward to further updates from Sanofi in due course. On slide 8, let me summarize the progress we are making with lacutamab, an anti-KIR3DL2 antibody. In T-cell lymphoma, we continue to pursue a fast-to-market strategy in the niche indication Sézary syndrome, where lacutamab was granted US Fast Track Designation and EU PRIME Designation in 2020. We have expanded past Sézary syndrome to mycosis fungoides, and we have seen encouraging preliminary data from our phase 2 trial in both diseases. Dr. Porcu will cover the data on Sézary syndrome shortly. On the mycosis fungoides cohorts, also included in TELLOMAK, we are eagerly anticipating final data due in-house by the end of the year, and we aim to share the data in the near future. Finally, we continue to follow patients with refractory relapsed peripheral T-cell lymphoma in the phase 1 B with lacutamab monotherapy. Enrollment continues in the study, in the randomized phase 2 with lacutamab in combination with chemo sponsored by LYSA. We announced earlier in the year that the U.S. FDA placed lacutamab IND on a partial clinical hold due to one case of hemophagocytic lymphohistiocytosis in the TELLOMAK trial. We have responded fully to the FDA requests, which include incorporation of risk mitigation and management strategy for HLH in ongoing lacutamab studies. We've carried out an in-depth analysis of the case together with a steering committee with independent experts, which point to the fact that the fatality is related to the aggressive disease progression and lacutamab unrelated. We await a resolution of the hold as we continue to cooperate with the FDA on this matter. On slide nine, I will now hand over the call to Dr. Porcu, who will update us on the TELLOMAK trial. Over to you. Thank you very much. Thank you, Sonia, for the introduction, and everyone, welcome. I'm very happy to present the data on lacutamab in patients with relapsed refractory Sézary syndrome, final results of the TELLOMAK phase two study. This presentation was given on Saturday, as Sonia mentioned, to a packed room with a lot of lymphoma investigators all over the world. Next slide, please. These are the investigators on the TELLOMAK trial. Next slide, please. Lacutamab, as shown in the cartoon on the right, is a first-in-class humanized anti-KIR3DL2 cytotoxicity-inducing antibody that is in development for the treatment of patients with cutaneous T-cell lymphoma, particularly mycosis fungoides and the Sézary syndrome, as well as, as Sonia mentioned, peripheral T-cell lymphoma. Now, Sézary syndrome is a rare, aggressive, T-cell malignancy, with very poor outcome and a high unmet need. And at the moment, there is no approved therapy to fail, or have received mogamulizumab. A phase 1 trial with Sézary syndrome patients who have received at least 2 prior systemic therapies, show that global overall response rate of almost 33% and a median duration of response of 13.8 months, with a median progression-free survival approaching 1 year. Based on this data, the drug received orphan drug designation from the treatment of CTCL, and then received PRIME and Fast Track designation, for Sézary syndrome patients treated with at least 2 prior systemic therapies. Next slide, please. TELLOMAK is an international multi-cohort, Phase 2 trial of a single agent, lacutamab, in two CTCL subtypes, shown here. And the drug is given intravenously, weekly for 5 weeks, then every 2 weeks for 10 doses, and then every 4 weeks until disease progression or unacceptable toxicity. Cohort one enrolled patients with Sézary syndrome, with at least 2 prior systemic therapies, one of which had to be mogamulizumab. Eligibility criteria are listed in this slide. Essentially, relapsed refractory advanced stage CTCL, B2 blood stage involvement, and patients had to have no evidence of large cell transformation based on central histological review. The primary study endpoint is global overall response rate, and there were a number of secondary endpoints listed in this slide. Next slide, please. This shows the patient characteristics at baseline with a total number of patients enrolled, 56, and the median age was 69. The median follow-up was 14.4 months. The distribution between males and females reflect the distribution of the gender distribution in this disease in the real world. All patients had advanced stage, all patients had the B2 blood involvement, and approximately 70% of the patients had lymph nodal involvement. The median number of prior therapies was five, and once again, all the patients enrolled had to have prior mogamulizumab. Next slide, please. This slide summarizes the efficacy results based on global response and then compartment response. I wanna start with the best global response, on the left column here, they're showing an overall response rate of 37.5%. Then moving on to compartment responses, which are very important, in treatments in development for CTCL. The best response in the skin overall response rate was 46.4%, and the best response in blood was 48.2%. I like to point out the depth of responses in blood with 15 patients, 26.8%, achieving a CR. There were also quite encouraging responses in the lymph node compartment, which is notoriously difficult in this disease, with approximately 20% overall response rate, including three complete responses. Next slide, please. Now, focusing now on global overall response on a waterfall plot here in looking individual patients, remarkable once again the fact that there were deep responses with 2 CRs and 19 PRs. The high global overall response rate really reflects multi-compartment efficacy here. It's notable that many of the PRs were very deep, and many of them were almost complete responses. The median time to global response was 2.8 months. Next slide, please. Responses were also durable, and this slide shows that the median duration of response for the responders was 12.3 months. Looking at the patients' sustained response at six and 12 months, the percentage was respectively 74.1% and 61.7%. Again, emphasizing that responses in these patients were durable. Next slide, please. Now, this slide focuses on, in depth on the blood responses. On the left is a waterfall plot for showing individual changes in blood tumor burden in patients. Once again, displaying the significant depth of responses with 27 patients, about 48.2%, achieving a blood response. Again, 15 patients achieving a complete response with a very rapid median time to blood response of 1 month. We also like to point out that there was one patient who had an unconfirmed CR who then went on to achieve a confirmed CR after the data cutoff. The panel on the right. And I apologize. Can you move to the next slide? Sorry, Sonia. Thank you. This is the slide I'm talking about now. My apologies. This is a blood response. So once again, on the left is a waterfall plot according to changes in response in blood response. The panel on the right, it shows the responses according to KIR3DL2 status and with the best blood response and best global response. And I think what's notable here is, first, that, KIR3DL2 expression on circulating tumor cells was found in all patients to, to a degree, and that in the vast majority of the patients, 92.3%, the median KIR3DL2 expression was very high. Looking at the expression KIR3DL2 and response, there was a greater number of responses. Most of the responses occurred in patients who had high level of KIR3DL2 expression, although there were patients who also had responses, even with a low level of expression on KIR3DL2. Now, moving on, I guess, back, Sonia, thank you, on the responses by compartment in the skin. On the left is a waterfall plot showing that the 46.4% of the patients achieved the skin response. Responses also in the skin were deep, not as deep as in the blood, but quite deep nonetheless, with 5 CRs, 21 PRs. Again, many of the PRs were very, very deep. The median time to skin response was 2.8 months. The panel on the right, it emphasizes the fact that when we look at the subset of patients who had high level of expression of KIR3DL2 in skin, first, we see that 87.5% of the patients had greater, equal or greater than 1% expression of KIR3DL2. And if we look at this group, and we compare the pattern and the breakdown of responses between that group and the entire study population, the pattern response is very similar. There's no significant differences. Patients out of this whole cohort had less than 1% expression of KIR3DL2. If we go back now to the left, looking at the patients noted with a blue asterisk, you can see that even in those patients with less than 1% expression, there were responses, including very good responses. Next slide, please. Next slide. Thank you. So now on to the progression-free survival, which is shown in this slide. It's with a fairly mature follow-up, once again, 14.4 months of median follow-up on this cohort. The progression-free survival was 8 months. And looking at different benchmarks here on the curve, there were patients at 12 months and 18 months that were still alive without progression, with 43.3% at 12 months and 38.9% at 18 months, which is quite a respectable progression-free survival for this disease, including the fact that all these patients had received prior mogamulizumab. Next slide, please. Now, this slide summarizes the safety data from the TELLOMAK. And I like about 50%, 57% of the patients experienced any lacutamab-related adverse event with the four listed here. General disorders of administration site conditions, skin, GI, and laboratory investigations representing the most common lacutamab-related adverse events. The one thing I'd like to point out here is that the frequency of skin and cutaneous reactions in this population with lacutamab was low, which is important in the context of the existing standards of care. In terms of serious adverse event, there were a few serious lacutamab-related adverse events. Three led to a discontinuation of lacutamab, with the causes listed in the notes. There were three death. I mean, three death related to adverse events, but none of them was lacutamab related. Next slide, please. This slide provides a summary information on two of the patients enrolled on the TELLOMAK, primarily to give an idea of the patterns of responses, including nodal responses, which once again are particularly challenging in this disease. So the first case on the left is a 58-year-old woman with 10 prior lines of therapy, who was advanced stage, of course, and also had a biopsy-proven lymph node involvement, defined as N3. This patient is currently on ongoing therapy with a sustained global CR at week 117. What's remarkable about this patient is the fact that she achieved a rapid complete response in blood at week 5, and then an initial partial response in both lymph nodes and skin evolved gradually, but reasonably rapidly as well to a complete response in the lymph nodes at week 13 and in the skin at week 45. The patient on the right is a 51-year-old woman with prior therapy, also advanced stage, also biopsy-proven lymph node involvement. And she is a sustained global CR at week 29. What's remarkable about this patient is the fact that in addition to a very rapid response in blood, complete response in blood, this patient was shown by the PET scan images there also had a complete response in the lymph nodes at week 5. And the skin response also evolved, again, from a partial response at week 5 to a complete response at week 13. So in conclusion, TELLOMAK is a phase 2 study evaluating monotherapy with anti-KIR3DL2 antibody lacutamab in CTCL. Cohort 1 enrolls patients with Sézary syndrome with at least 2 prior lines of therapy, one of which had to be mogamulizumab. This is a very high unmet need patient population with no approved therapy post-moga. If we look at the 56 patients enrolled in the analysis at data cutoff, there is evidence of very good clinical activity with a favorable safety profile. Safety, in particular, confirming the initial data from the phase 1. And these patients were heavily pretreated with a median of 5 prior therapies. As shown in the slides, responses were as noted across all compartments, which is extremely important, including CRs in all compartments. And then in patients who achieved a global response, responses were rapidly, not just in the blood, but also in the skin. And the median duration of response was 12.3 months. The enrollment, as we announced in the summer, in Lugano, the enrollment to TELLOMAK is now completed. The patients are being followed, of course, and as they do, additional data will lead to more mature assessment of these key study endpoints. Next slide, please. So TELLOMAK was a remarkable, international collaboration, that really, supported-- is supporting, the development of, new drugs, new investigational therapies, in a very rare, malignancy, hematologic malignancy, for which there are no good, standards of care at the moment after, mogamulizumab. So this is remarkable, and this has been only possible thanks to collaboration of, multiple sites, both across Europe and the US, and the sites are listed here.... We also want to thank all the patients and their families, all the investigators, and the site staff. This study is sponsored by, Innate Pharma. Thank you very much. I'm happy to take any questions, with Sonia here on this call. Thank you. If you have a question, please press star one on your telephone keypad. If you wish to remove yourself from the queue, simply press star one again. One moment, please, for your first question. Thank you, Dr. Porcu, for the excellent presentation. I will now continue by providing a summary, and then we can take questions. Now, as you can see on slide 26, we continue to work diligently to execute across all our strategic pillars and believe that we are laying the foundation to drive near and long-term value. Looking at our clinical stage programs, we expect to achieve a number of milestone over the next two years. We have covered the lacutamab phase 2 TELLOMAK in Sézary and anticipated mycosis fungoides data, which is imminent. In parallel, we continue to develop our ANKET platform, further reinforced by our partner, Sanofi, and we are very encouraged by the initial clinical data presented at Congress this year and the IND clearance for our proprietary ANKET and progress in the clinic. For monalizumab, the lung cancer trials are proceeding well, and we continue to advance the adenosine pathway agents in the clinic, where the phase II for IPH5201 in early lung is underway. Now, let's move to the conclusion slide. On the final summary slide, as you can tell, we continue our exciting journey at Innate. We look to build our business to create value for patients and stakeholders. In summary, we have positioned Innate Pharma for the future with our strategy and made meaningful progress across all strategic pillars. With our R&D engine and antibody engineering expertise, our science is producing more candidates to the clinic. Some we are developing alone and some partnered. We have a focus on NK-cell engager platform, the ANKET, as well as ADC. And in parallel, our late-stage portfolio continues to advance as we look to maximize our late-stage assets, lacutamab and monalizumab. Our partnership strategy continues to evolve, with Takeda deal adding to those already existing with AstraZeneca and Sanofi. We have carefully managed our resources so we can continue a sustainable business to invest in progressing our pipeline, and I'm very pleased that we continue to have a strong cash position with a runway into the second half of 2025. Collectively, we are driving value across our business and ultimately advancing our goal to deliver innovative medicine to patients. We look forward to keeping you updated on our progress, and now I will hand over to questions. Thank you. Thank you. And again, if you would like to ask a question, press star and the number one on your telephone keypad. Your first question comes from the line of Daina Graybosch of Leerink Partners. Your line is open. Yeah, I have a couple questions for the doctor. Dr. Porcu, I wonder, as you look forward and think about, think about the next trials you might do with lacutamab in T-cell lymphoma, as the company will have to do one for confirmation of regulatory approval, I wonder what kind of designs would be top of the list for you? Yeah, thank you. That's a great question. And I think that it's a complex conversation that will have to include both considerations about, you know, science and the data and also considerations about, you know, the regulatory path that the FDA may sort of lay down for us. Obviously, I, I'm not in a position to discuss that particular component on for Innate. I can say that is fluid and, you know, unclear. One thing that we all know is that the FDA historically, you know, recently, has been focused on emphasizing the importance of randomized trials with a comparator. I think that, you know, the complexity here is gonna be that, the selection of a comparator that I think is gonna be, meaningful, in a patient population that, for example, like in this case, with Sézary syndrome, that, had received already the c- the comparator. And, you know, as a, as an investigator, looking, you know, forward to, see the, the ex- the development and, and the accelerated development of, drugs, for this patient population, I think that, the design of, the lac- TELLOMAK, by requiring the, the having been exposed to tel- to mogamulizumab be- before, to me, that is a very strong... It's a very strong feature of the trial because it really kind of offers a very strong value in terms of the, you know, response efficacy, and you know, both in terms of response, duration, as well as progression-free survival. So looking at what the next study may be, the next best study may be. I don't think I'm in a position right now to say because we're gonna have to see, first of all, the continuation of the final, you know, efficacy on the TELLOMAK as more follow-up accrues. And then see what the FDA is going to sort of analyze in terms of proposals for the confirmatory study. So it's a very, very dynamic and exciting moment right now to look at the final development of lacutamab. Thank you. One more follow-up from me is- Yeah. There's been a lot of changes in the endpoints in, Yeah ... this indication over time, and there's yet another one, which, you know, hasn't been used in this trial because this trial started before that. As you look across all these endpoints, which endpoint for you in your clinical practice do you look to that you think best exemplifies the clinical benefit that you see in patients, in front of you? Yeah, that's another great question, really. So I agree that there has been a lot of shift and changes in, you know, the primary endpoints or the studies, for example, you know, the CR, overall response for, you know, like for the ALCANZA trial, progression-free survival for MAVORIC, global overall response rate here for TELLOMAK. I would say that the most clinically relevant endpoint, the changes depending on the disease. So for example, if you look at CTCL overall, certainly the durability of the response or potentially progression-free survival is an important endpoint. As complex as it is because for CTCL, you know, progression-free survival can be fairly challenging to define. Now, for Sézary, though, which is the data that I presented today and we presented on Saturday, I think that we're. The depth of the responses are really the, in my view, the most important endpoint because, you know, we know that it has been very difficult to achieve deep global responses where the drug is affecting all compartments of the disease. And without in the absence of those deep global responses, we know that the meaningfulness of the responses and the clinical benefit is not great. So it to some degree depends on the specific subset that we're looking at, and that adds complexity to a global, you know, assessment from your standpoint, for example, of what's the value of all these different drugs is. Great. Thank you very much. My pleasure. Your next question comes from... Your next question comes from the line of Yigal Nochomovitz of Citigroup. Your line is open. Yeah, hi. Thank you for taking the question. For Dr. Porcu, you mentioned that there were some responders in the patients that had very low KIR3DL2 in the assay. Can you just comment on the explanation for how those would respond, or may it have been something with the assay that didn't completely reflect the expression because they, you know, they just did a bad sampling, and actually, they did have higher KIR3DL2 than the assay would suggest? Right. Yeah, that's also a good question. That's something that Innate is, you know, obviously looking at very carefully internally. Just as an investigator, not being part of the team that is actually doing these assays, I can say that, number one, just for like any biomarker, if you look at any biomarker for targeted therapy in development or recently developed, there are always, you know, there's always a spectrum of expression of the biomarker, and typically, you will see responses also at low levels. The best example perhaps is CD30. That's number one. Number two, here, you know, the biomarker in different compartment because one thing is skin, another one is blood. You know, the assays are different, obviously, in blood and skin, and the antibodies used are also different in blood than skin. And these are snapshots, of course, of expression at one time point. And then because of... in general, including Sézary, is really a multi-compartment, Hi. Apologies, we seem to have lost Dr. Porcu. Bear with us while we just try and reconnect him. In the meantime, Yigal, do you have any further questions for Sonia, or we can wait till we reconnect? Sure. I just wanted to check on the, well, kind of on the comments before around the filing strategy. Is the plan to speak to the FDA once you have the final MF data about accelerated approval? Is the expectation that that's the, like, the outcome, or you don't know yet and you need to talk to them? Absolutely. The plan is to have the MF data that are going to be the top-line results are going to be in-house by the end of this year, and then approach the FDA. And also, as Dr. Porcu outlined, you know, with the previous question, any accelerated approval must present a confirmatory trial, and we will discuss with the FDA around the confirmatory study design, the patient population that is going to be part of the study design, whether it's a Sézary plus mycosis fungoides or Sézary alone, and the comparator arm. And so this is something that we will be able to define only after we had this interaction next year. And then one other one, Sonia. Just with this study, what was the requirement in terms of the MOGA washout time? I'm just curious if there was... What the half-life of MOGA is, and if there's- Right. -any thought that- Now, all patients- Would be pertinent or not? Yes, all patients received mogamulizumab as part of the inclusion criteria. However, there was a five weeks washout period prior to enter the study. Okay. Yeah. Thank you. Now, going back to your question, unfortunately, we have lost Dr. Porcu, that he was addressing the question of the KIR3DL2 expression in different compartment, and of course, the assays are also different. Sometimes what you see and what was presented in the slides is the expression level at baseline. Now, we know that on therapies, lacutamab can upregulate the expression of KIR3DL2, and so it is not uncommon, and also this is a target that can be upregulated on tumor cells, and therefore, it's not uncommon to see movement, let's say, either upregulation or downregulation, depending on the different stages of disease. It seems we have back Dr. Porcu? Yeah. Hi, Sonia. Hi. Sorry, everyone. For some reason, my connection got lost, but I'm on with my phone. If you can hear me okay, I'm happy- Yes, we can hear loud and clear. Okay. Thank you. I mean, I think you answered all the questions, you know, Sonia, that I think- Yeah, Luigi, I don't know if you wanted to conclude on the KIR3DL2 expression because we lost you at that time. You were talking about- Okay ... a KIR3DL2 expression in the different compartments, skin and blood. I don't know if you wanted to add on that because we lost you at that point. Yeah. Thank you. No, sorry. So I think that's a key thing, really, that, you know, that, you know, it's when we look at the expression at entry, it's, you know, looking at any one compartment, the expression can be slightly different. So I'm not, you know, I'm not either surprised or sort of concerned that, you know, this, the fact that we are seeing a few respond. The majority in the blood, the majority of the responses were seen in patients who had, you know, a high level of expression, and the vast majority of them did. So I think this is just normal. I would say, I would call it background noise for kind of biomarkers. And, regarding the fact, Sonia, that you mentioned, that it is possible, even that, you know, the expression of KIR3DL2 in one or more compartment may actually change, as treatment goes on, and therefore, that could also affect the response. I think at this point, we don't know for sure. I mean, I think that's a good hypothesis based on some data that I understand are available. And therefore, that would be definitely worthwhile exploring further, because if it is, that actually would be quite a remarkable additional angle in terms of lacutamab, for this patient population. Your next question comes from the line of Liisa Bayko of Evercore ISI. Your line is open. Hi. Hi, thanks for taking the question. For PTCL, can you give us a sense of when, you know, when we're gonna have data there, that sort of gives us an indication of advocacy? You will take this, Sonia. Sure, sure. For PTCL, we have a study, an IST study with cooperative group, and the study will provide some data in 2025. This is a PTCL in combination with GEMOX. Okay, great. Thanks. And then for the MF study, you know, what are your expectations, and what would your be your interpretation of, you know, the differences between cohort two and cohort three, and sort of, you know, responding in one of these populations that is either positive or negative for the biomarker? Do you... Again, just talking about noise, and you mentioned in your prior comment, would you see that more as kind of noise based on maybe some similar consideration to Sézary or, you know, compartment-related, or how are you thinking about sort of the- Right ... interpretation, the implications for PTCL, for example? This is a great question. Yeah. In one way. ...Dr. Porcu, would you like to take the question, or am I on? As you wish. I'm happy. Okay. As you wish, Sonia. Yeah. I'm happy to take a stab at it, and then you can, you can sort of pitch in, you know. Yeah. I can—at least I can give you my perspective on this, and then Sonia can give her perspective. I mean, it—I would say as an investigator, you know, I would say this, one, that the analysis of the expression of KIR3DL2 in the skin or any other biomarker, it's a little more complex than the expression in blood. Because in blood by flow, it's fairly easy to look at, you know, the population that you're looking at in terms of, both you can do it both by gating, as well as by, you know, additional antibody markers. So it's much more clean in the blood by flow cytometry. In the skin, you know, you have to look at, you know, it's a complex environment, you know, microenvironment there, you know, a lot of different cells. Sometimes identifying the tumor cells may not be immediately, you know, obvious or easy. Therefore, when we look at the expression of any biomarker in the skin, I would say we always have to be a little, you know, cautious, particularly in terms of interpreting differences between levels of expression and then correlating those differences to outcomes. So to kind of then to go to your question, I would say that, you know, it's pretty obvious that the expression of KIR3DL2 in MF is positive in, I believe, Sonia, correct me if I'm wrong, but I think it's about 50% of the MF patients express KIR3DL2. And this is, you know, as opposed to Sézary, where the expression is much higher. In fact, all patients expressed some KIR3DL2, and the vast majority of them expressed a very high level of KIR3DL2. So with that in mind, I think that we will, you know, we will see what the responses, you know, the final responses to lacutamab in MF are. I think that, you know, Innate has this cohort, you know, the all-comers cohort, that the purpose of the cohort is exactly to see, you know, to have a whole spectrum of expression of KIR3DL2 and see how responses are gonna be in that cohort. So I'm waiting as an investigator and clinician, I'm waiting to see the final results of the MF cohort. I don't necessarily hang my hat on the fact that, you know, patients have to be strongly KIR3DL2 positive to respond, and whether there is a cutoff or a threshold. At this point, I don't have any data to really support that's the case. We're just gonna have to be driven by what the data show. Sonia, do you wanna, do you wanna add something? Thank you, Luigi. It was brilliant. I don't have anything to add. Okay. Your next question comes from the line of Swayamp akula Ramakanth of HCW. Your line is open. Thank you. Most of my questions have been answered, but I have one question to Dr. Porcu. As an investigator, when you're looking at all the data that you have at hand, from the study in Sézary syndrome, and when you compare it against what you're, what you have seen so far, is there any piece of data that you feel you still need to get your hands on in order to kind of internally, just for yourself, to make a decision on how you would want to use this in your clinic? Yeah, that's also a great question. Well, I mean, so when we're treating patients in the clinic, we always—the calculation always is a balance between efficacy and safety. So, you know, I would say the efficacy/safety equation and balance, at the end of the day, that's really kind of the most important decision, you know, or item that we have to look at. So with that in mind, I feel already pretty good about lacutamab in patients with Sézary syndrome, specifically, which I think that's your question, but in general, also for MF. You know, the safety of lacutamab is based on the phase 1 that was already published, and then now the phase 2. I think, it's very good. I would go as far as to say that it is, you know, competitively good, you know, in respect to the existing standard of care, because, you know, there are, and you know, well, to be explicit, mogamulizumab, which is an approved drug, so we can talk about it. You know, and mogamulizumab has a number of adverse events that can be concerning. We know one is the MAR, you know, the Moga-associated rash, which may not be severe from a medical standpoint necessarily, although sometimes it can be, but it's quite a handful because patients, you know, require often steroids, you know, they cannot resume therapy. So it kind of is really a significant sort of burden. And in addition to that, there are also less common but still observed immune-mediated effects from Moga. And so based on all the data that we have so far, we don't see those with lacutamab. I mean, obviously, it's still early, and, you know, the drug is not in the market yet, and a lot, you know, a lot of things can happen after the drugs can get used in the market. So but, for now, I think that is an important part of the calculation. Efficacy-wise, as I mentioned, you know, it, to us, as clinicians, we really need to see complete responses across all compartments. And one of the strengths of TELLOMAK is that the quality of the data on nodal responses in particular is significantly better than the quality of the data that we had with all prior therapies. And so based on that, I don't feel that I have to kind of wait for anything major at this point, and except for the data in Mycosis Fungoides that still have to mature, and I think we wanna know. Does this address your question? Yep, yep. Thank you very much- Okay. for that, doctor. Okay, my pleasure. Okay, we've just got a couple of questions, online as well. So maybe for Sonia, I'll bundle them together just on the regulatory strategy. So do you anticipate to file in the U.S., and the E.U.? And also thinking about, you know, the TELLOMAK trial was in heavily pretreated patients. Given the results, do you think it's possible to go in an early line setting against MOGA or earlier disease? Well, I think in a way, all these questions have been kind of addressed by some of the questions before. Of course, it's they are important questions, but as Pierluigi just mentioned, the favorable safety profile of lacutamab, together with the efficacy, the depth of the response that we have seen from the phase 1 together with the phase 2 can really point to the fact that the lacutamab can be used also in earlier line. Of course, this this needs to be discussed with the regulators, and depending on what the control arm could be, it's not impossible to see also a registrational trial in an earlier setting. And we will go for FDA discussion in early 2024. Okay, thank you very much. I don't see any further questions on the line or on the phones. So, sorry, one further question has actually literally just come in. So Eric Le Berrigaud at Stifel. Two questions for Dr. Porcu. Number one, by TELLOMAK design, patients had to be post-MOGA, and therefore, second-line plus, but the reality is that patients had received four-line plus on average. Can you let us know how and when you're using MOGA in your daily practice? Which patients? What stage? And the second part is, considering the risk-benefit balance seen in TELLOMAK, would you say it may be a loss of chance for patients not to be used earlier than fifth line when available? So, for Dr. Porcu. Yeah. Thank you. Yeah, thank you. Great question. So, in terms of now the real-world use of mogamulizumab in patients with CTCL, definitely is being used earlier on, particularly in patients who have blood involvement, which, you know, is defined as not necessarily B2, but also B1. And it's something that now in practitioners, you know, across the world are assessing more and more in patients with CTCL. And there are data now that are accruing and being presented looking at how MOGA is being used in the real world, and it's true that it's being used earlier on. So, certainly, I would say that, you know, the same pattern could easily be projected for lacutamab. You know, I would imagine that, we would not for patients, particularly for patients who have blood involvement, again, pending the final data for MF, which at this point, I don't think we can kind of make any meaningful comment on. But for Sézary patients with blood involvement, I think that the drug, if lacutamab were available, you know, people would use it much earlier. The median number of prior therapy was five, actually, in the Sézary cohort. So, yeah, we definitely would use it earlier, and this is gonna be a pattern, I think, for most, you know, active drugs moving forward, with in this space. Okay. Now, I don't see any further questions on the line or on the chat. So, Dr. Porcu, thank you very much. Thank you very much, everyone, for joining today. Dr. Constantino, thank you, and have a good rest of your day. Thank you. Okay. Thank you, everyone. Okay. This concludes today's conference call. You may now disconnect.