Ladies and gentlemen, thank you for joining us, and welcome to the Innate Pharma full year 2025 earnings call. After today's prepared remarks, we will host a question and answer session. If you would like to ask a question, please raise your hand. If you have dialed into today's call, please press star nine to raise your hand and star six to unmute. I will now hand the conference over to Stéphanie Cornen, Vice President of Investor Relations, Communications, and Commercial Strategy at Innate Pharma. Please, Stéphanie, go ahead. Thank you. Good morning and good afternoon, everyone, and thank you for joining us for Innate Pharma's full year 2025 business update and financial results conference call. The press release and today's presentation are available on the investor relations section of our website. Before we begin, I would like to remind everyone that today's presentation includes forward-looking statements based on current expectation. These statements involve risk and uncertainties that could cause actual results to differ materially. I will briefly cover today's agenda. Our CEO, Jonathan Dickinson, will begin with a strategic overview and outlook. We will then share updates on our three priority program, lacutamab, IPH4502, and monalizumab, as well as IPH5201 in partnership with AstraZeneca. Speakers will be our CMO, Sonia Quaratino, our COO, Yannis Morel, and I. Frédéric Lombard, CFO, will comment our financial results. Jonathan will return with upcoming catalyst and closing remarks before we open the call for Q&A. With that, I'll now hand it over to Jonathan. Thank you, Stéphanie. Good morning to those joining from the U.S., and good afternoon to our European audience. Turning to slide five, Innate Pharma is a focused oncology company with a clear ambition to deliver high-value differentiated therapies for patients with significant unmet medical need. Our strength lies in our deep expertise in antibody engineering and our ability to translate this into innovative therapeutic approaches, particularly in immuno-oncology and antibody-drug conjugates. Over the years, we have built a pipeline of highly differentiated assets built on targets we believe have high potential to deliver meaningful clinical benefit. Today, we're focused on advancing these assets through late-stage development, combining smart, agile execution with a clear line of sight to key clinical and regulatory milestones. Turning to slide six. Over the past year, we have taken important steps to deliver on our strategic priorities with an execution-driven organization. As we announced previously, we made the decision to prioritize investment on what we believe are our three highest value clinical assets, IPH4502, lacutamab, and monalizumab. This strategic focus allows us to concentrate our resources where we see the greatest potential to generate clinical impact and long-term value. In parallel, we continue to leverage our internal expertise and platform capabilities to advance the next generation of ADCs. At the same time, we have streamlined the organization to ensure we are fit for purpose, with a more agile structure that supports efficient decision-making and disciplined capital allocation. As previously communicated, we implemented a redundancy plan, which is expected to be completed by the end of April. Turning to slide seven. We continue to execute against our strategy with discipline across our core programs and are pleased with the strong progress we are seeing. First, as you remember, we received the FDA clearance to proceed with the TELLOMAK 3 phase III trial with lacutamab in CTCL, and we expect to be able to initiate it in the second half of 2026. In parallel, we are actively advancing discussions with ongoing negotiations on several fronts, including potential pharma partnerships and royalty-based structures. We believe these approaches provide a disciplined path forward to support late-stage development while preserving shareholder value. Second, we're advancing IPH4502, our novel Nectin-4 ADC, where we see the potential to deliver a differentiated profile and address significant unmet needs across multiple tumor types. IPH4502 is progressing rapidly with early signs of antitumor activity in heavily pretreated patients, including in urothelial cancer previously treated with EV, and a favorable safety profile seen to date. We are starting to validate our preclinical hypothesis, which supports a differentiated profile versus MMAE-based approaches. We are currently enriching cohorts at pharmacologically active dose levels in urothelial cancer post EV, and selected additional tumor types, and are excited by the progress we are seeing to date. Third, monalizumab, in partnership with AstraZeneca, represents an important late-stage asset with the PACIFIC-9 phase III trial data readout expected in the second half of 2026. Across these programs, we remain focused on driving value, prioritizing key milestones, and ensuring that we are well-positioned to deliver multiple catalysts over the near and medium term. With that, I will now hand it over to Sonia. Thank you, Jonathan. Now, moving to slide nine and starting with lacutamab, our late-stage asset in cutaneous T-cell lymphoma. As a reminder, the phase II TELLOMAK study has demonstrated a clinically meaningful and durable activity in both mycosis fungoides and Sézary syndrome, including improvement in quality of life with a favorable safety and tolerability profile, supporting potential for long-term treatment. Building on this data, first, we have established a strong regulatory foundation, obtaining Breakthrough Therapy designation in relapsed or refractory Sézary syndrome, as well as Fast Track, PRIME, and Orphan Drug Designation. Second, this data support the potential accelerated approval path in Sézary syndrome, the most aggressive CTCL subtype characterized by high unmet medical need and no standard of care after treatment with mogamulizumab. Lastly, we have received FDA clearance to proceed with the TELLOMAK 3 study, which intends to be a confirmatory study for Sézary syndrome and the registrational study for mycosis fungoides. The initiation of TELLOMAK 3 is planned for the second half of 2026 as we evaluate financing options. In slide 10, I will now walk you through the phase III trial design. The proposed phase III study, TELLOMAK 3, is an open-label, multicenter, randomized comparative study to demonstrate the efficacy and safety of lacutamab in two separate cohorts of patients with cutaneous T-cell lymphoma who have failed at least one prior systemic therapy. In cohort one, there will be patients with any stage SS who have failed at least one prior line of systemic therapy, including mogamulizumab. Patients will be randomized 1:1 to either lacutamab or romidepsin. In cohort two, patients with MF from stage Ib to stage IV who have failed at least one prior line of systemic therapy will be randomized 1:1 to either lacutamab or mogamulizumab. Both cohorts will be randomized 1:1, and randomization will be stratified according to disease stage and region. The primary endpoint for both cohorts is PFS by blinded independent central review. The secondary key endpoint for the SS cohort is overall survival, while the key secondary endpoint for mycosis fungoides are quality of life and pruritus. As the Sézary syndrome and mycosis fungoides study subpopulation are considered as independent cohorts answering to distinct objectives, two sample size are estimated to meet the primary endpoint in both SS and MF cohorts independently. As such, the study's power to demonstrate superiority of lacutamab effect on PFS as compared to romidepsin in patients with SS who received at least one prior line of systemic therapy, including mogamulizumab, and that's compared to mogamulizumab in patients with MF who received at least one prior line of systemic therapy. From a regulatory standpoint, we have received FDA clearance to proceed with this clinical trial protocol, and we are now progressing towards phase III initiation expected in the second half of 2026. Slide 11 outlines the projected regulatory timelines for lacutamab in Sézary syndrome and mycosis fungoides. As previously presented, the phase II TELLOMAK data in Sézary syndrome are intended to support a potential accelerated approval once the confirmatory phase III trial is underway. In this context, the TELLOMAK 3 study is designed to serve as a confirmatory trial for SS, while also supporting full approval in mycosis fungoides. In the MF cohort, the primary endpoint of progression-free survival is expected to support full approval in both U.S. and Europe. Importantly, given the larger patient population in mycosis fungoides, we expect enrollment in this cohort to be faster, which may enable an earlier completion of the primary analysis in this indication. From a regulatory standpoint, this represent a stepwise development approach, starting with Sézary syndrome with the highest medical need, and then expanding into broader CTCL population. From a commercial perspective, we see a focused and attractive opportunity for lacutamab in CTCL, starting with Sézary syndrome. Based on recent real-world data analysis, we estimate approximately 300 incident patients per year in Sézary syndrome in the U.S., with a prevalence of around 1,000 patients, the majority of whom are treated in a limited number of specialized academic centers. Importantly, this is a highly concentrated treatment landscape, with over 85% of patients managed in academic centers and a large proportion treated within approximately 50 key institutions. This concentration enables a targeted commercial approach with limited infrastructure. At the same time, Sézary syndrome and mycosis fungoides share the same prescriber base, which is a critical point from a commercial perspective. This means that an initial launch in Sézary syndrome is not a standalone opportunity, but a direct entry point into the broader CTCL market. Mycosis fungoides represents a significantly larger opportunity with approximately 3,000 incident patient per year and the prevalence of around 12,000 patient in the U.S. Importantly, when looking at the current market, mogamulizumab generated approximately $300 million in annual sales in 2025 as planned, and is projected to reach $350 million in 2026, with strong adoption in Sézary syndrome and more limited penetration in mycosis fungoides. This provide a relevant benchmark for the market opportunity and highlight the potential for a therapy able to capture share across both Sézary syndrome and mycosis fungoides. From a value perspective, the key driver include treatment duration, supported by the durability of response, pricing, and market share across a broader eligible patient population. Taken together, this supports a stepwise commercial strategy, starting with an initial opportunity of up to EUR 150 million in Sézary syndrome, expanding to over EUR 500 million across Sézary syndrome and mycosis fungoides in the second-line setting, with additional upside as lacutamab moves into earlier lines of therapy and broader patient segments over time. With that, Yannis and Sonia will now walk you through IPH4502. Thank you, Stéphanie. Turning to slide 14. On this slide, I would like to highlight why we are particularly excited about our next-generation Nectin-4 ADC program called IPH4502. As mentioned earlier, IPH4502 is a differentiated ADC built to improve both safety and efficacy through a novel design. This molecule is based on a proprietary humanized antibody that bind on the Nectin-4 target to a distant and non-overlapping epitope versus enfortumab. It is combined with a stable, cleavable, and hydrophilic linker, which supports high systemic exposure of the ADC while minimizing the release of free exatecan in the circulation, and therefore reducing the risk of off-target toxicity. The payload, exatecan, is a potent topoisomerase I inhibitor with strong bystander activity, enabling it to target not only Nectin-4 expressing tumor cells, but also neighboring cells with lower or heterogeneous expression. Importantly, IPH4502 has demonstrated activity in models resistant to enfortumab vedotin, supporting its potential to address tumors that are either refractory to or progress after current standard therapies. Overall, the design of IPH4502 is intended to overcome key limitations of third-generation Nectin-4 ADCs and to deliver a more favorable therapeutic profile. Slide 15. Here, we position IPH4502 within the current Nectin-4 ADC landscape and highlights its key differentiating feature. As you can see, the majority of Nectin-4 ADCs currently in clinical development, including approved and late-stage assets, are based on MMAE payloads such as enfortumab vedotin or PADCEV. While these therapies have demonstrated clinical activity, they are also associated with certain limitations, particularly in terms of safety and resistance mechanism. In contrast, IPH4502 is based on topo I payload, exatecan, which we believe offers a differentiated mechanism of action. Importantly, this allows us to potentially overcome some of the limitations observed with MMAE-based conjugates, including activity in tumors that are resistant to or have progressed following enfortumab vedotin. Indeed, MMAE-based ADCs are largely developed in bladder first-line setting in direct competition with the approved standard of care, when the trial of IPH4502 includes patients relapsing after enfortumab vedotin. In addition, as mentioned earlier, the strong bystander effect associated with exatecan may enable activity in tumors with low or heterogeneous Nectin-4 expression, thereby broadening the potential addressable patient population. Taken together, we believe that IPH4502 combines a differentiated design with a competing mechanism, positioning it as a potential best-in-class topo I-based Nectin-4 ADC. Turning to slide 16. Here, we present new preclinical data supporting the profile of IPH 4502 as a potential best-in-class topo I Nectin-4 ADC. Starting on the left-hand side of the slide, in a CDX model with high Nectin-4 expression, IPH 4502 demonstrates strong antitumor activity as other topo I ADCs do. However, the key differentiation emerges in models with low Nectin-4 expression, where IPH 4502 maintains meaningful antitumor activity, while other topo I ADCs in clinical development show a clear loss of efficacy. This is particularly important as it highlights the unique ability of IPH 4502 to remain active in tumors with lower target expression. Overall, across multiple in vivo models, we consistently observe a differentiated antitumor profile for IPH 4502, supporting its potential as best-in-class agent, particularly in low to moderate Nectin-4-expressing tumors. We believe this profile is driven by the combination of a high-affinity antibody with a unique epitope, a stable and hydrophilic linker, and a strong bystander effect of exatecan. Now, handing over to Sonia, who will present to you the IPH4502 phase I trial. Thank you. Now let's turn to slide 17. IPH4502 is currently being evaluated in a first-in-human phase I study in patients with selected advanced solid tumor known to express Nectin-4. The trial is guided by an adaptive BOIN design with backfill cohorts with the objective to assess safety, tolerability and preliminary antitumor activity. The study runs at specialized cancer sites in the U.S. and in France. Enrollment in the dose escalation part of the study has progressed well. The maximum tolerated dose is currently explored, and we are enriching cohort at pharmacologically active dose levels, including patients with urothelial cancer, relapsed or refractory to enfortumab vedotin, as well as selected additional tumor types. We've started to observe preliminary antitumor activity in this heavily pretreated patient population. Importantly, the safety profile to date remains favorable. As the next step, we will build the package necessary to support the rationale for the dose optimization and selection of the recommended phase II dose. Now turning to slide 18. Based on the promising preclinical data we have generated that suggests that IPH4502 has robust activity in UC models resistant to EV, and we are focusing on patients with UC who progressed after EV treatment. Despite the significant progress EV has delivered in treatment of urothelial cancer, and most notably by nearly doubling survival rates when combined with pembrolizumab, challenges regarding resistance, side effects, and long-term remission persist. In the first-line setting, the majority of patients progress within two years, with approximately 63% experiencing disease progression within 24 months. On the right-hand side of the slide, we can see a fragmented treatment landscape and limited effective option for this patient, and this treatment landscape is still dominated by platinum-based therapies. This real-world data show that the outcomes in this setting remain poor, with time to next treatment of around three -five months and an overall survival in the range of seven-eight months with chemotherapy-based regimens. Taken together, this defines a clear therapeutic gap in the post-EV setting, and IPH4502 is designed to address the significant unmet need in this patient population. Turning to slide 19. Based on the profile of IPH4502 and the data generated to date, we see a clear opportunity to develop the program across multiple solid tumors. In particular, in metastatic urothelial carcinoma, we are initially focusing on the post-EV setting, where, as shown on the previous slide, there remains a significant and growing unmet need. In this context, IPH4502 has the potential to provide a new treatment option for patients to progress after EV-based therapies. Beyond this initial setting, we also see the opportunity to move earlier in the treatment paradigm, including into first-line setting, in combination with anti-PD-1 therapies. In parallel, we believe IPH4502 has the potential to be explored across multiple solid tumors beyond bladder cancer in tumors with low to moderate Nectin-4 expression. Overall, our objective is to build a broad and modular clinical development strategy, starting with high unmet need population and expanding into earlier lines of therapy and additional tumor types over time, depending on the emerging data. In slide 20, I will now turn to m onalizumab and IPH5201. Starting with monalizumab, the anti-NKG2A antibody co-developed with AstraZeneca. We remain focused on the progress of the phase III PACIFIC-9 trial in non-small cell lung cancer, a trial led by AstraZeneca, which represent the next key step in the development of monalizumab. The next slide, we see that this double-blind phase III PACIFIC-9 trial is designed to evaluate durvalumab in combination with either oleclumab, an anti-CD73 antibody, or monalizumab, an anti-NKG2A, compare to durvalumab alone in patients with resectable stage III non-small cell lung cancer who have not progressed following platinum-based chemoradiotherapy. This study builds on a strong scientific rationale supported by controlled phase II studies in early lung cancer, including COAST, NeoCOAST, and NeoCOAST-2. PACIFIC-9 is a large global trial that has now completed enrollment with approximately 999 patients randomized in a 1:1:1 ratio across the three treatment arms. The primary endpoint is progression-free survival with efficacy comparisons of both combinations versus durvalumab monotherapy. We now look forward to the data expected in the second half of 2026. Let's now briefly touch IPH5201 in the next slide. This is a first-in-class humanized blocking monoclonal antibody that targets CD39, an enzyme that plays a key role in suppressing the immune system within the tumor microenvironment. The ongoing MATISSE phase II trial is a multicenter, open label, single-arm study evaluating the combination of IPH5201 and durvalumab plus standard chemotherapy in patients with early stage lung cancer. The study is conducted by Innate in collaboration with AstraZeneca. We are happy to share that the results of a pre-planned interim analysis of this study have been selected for an oral presentation in a clinical trial plenary session at the AACR Annual Meeting in April in San Diego. Turning to slide 23, I would like to remind you the financial terms for both monalizumab and IPH5201, as our partnership with AstraZeneca represents an important upside for Innate. For monalizumab, the agreement amounts up to $1.275 billion of milestones. We already received $450 million and remain eligible to additional $825 million of potential payments. In case monalizumab is approved, AstraZeneca will book sales, and Innate Pharma will receive double-digit royalties on sales in U.S. and rest of the world. In Europe, as Innate Pharma is contributing to 30% of the funding for the phase III trial, we will get 50% of the profit and have the option to co-promote the drug. The agreement regarding IPH5201 is worth up to $885 million in milestones. To date, we already received $60 million and remain eligible for $825 million. This agreement, having a similar structure to the monalizumab one, Innate has also the option to co-fund phase III trials in order to get 50% of the profits in Europe and co-promotion rights. Otherwise, Innate Pharma will receive royalties in Europe, like in the U.S. and rest of the world. With that, I will now hand it over to Frédéric to walk you through the financial results. Thank you, Yannis. Now turning to slide 25, I will walk you through our 2025 financial highlights. Revenue and other income amounted to EUR 9 million this year. It includes EUR 2.8 million from licensing and collaboration agreements, primarily related to recognition of proceeds from our partnerships with AstraZeneca and Sanofi. As well as EUR 6.2 million in governmental funding for research expenditures. Operating expenses were EUR 63 million, of which 73% were related to R&D. R&D expenses were EUR 43.6 million, decreasing by 16% year-over-year, reflecting the study's maturity as well as decrease in indirect R&D expenses, primarily due to lower staff costs and reduced scientific consulting and IP cost. Partially offset by restructuring charges following the workforce restoring plan execution. G&A expenses were EUR 19.4 million, broadly stable year-on-year, with a decrease in non-scientific consulting fees and reduced insurance expenses, partially offset by the workforce restructuring plan impacts. Turning to our cash position, we ended the year with EUR 44.8 million in cash equivalents and financial assets as of December 31, 2025. Based on our current operating plan, this provides funding visibility until the end of the third quarter of 2026. With that, I will now hand it back to Jonathan for the closing remarks. Thank you, Frédéric. Turning to the next slide. As we close, I would like to highlight the strength of our focused portfolio built around three high-value assets, which are positioned to drive innate value. Starting with IPH4502, we are making strong progress in phase I. The study is progressing very well with high interest, and we are enriching cohorts at the pharmacologically active dose levels. We have observed preliminary antitumor activity with a favorable safety profile to date, including in patients with urothelial cancer, which are relapsed or refractory to EV, which is a signal that we're starting to validate the preclinical hypothesis. We believe IPH4502 has the potential to address the significant unmet need in the post-PADCEV setting, as well as the opportunity to expand beyond bladder cancer in low and moderate Nectin-4 expressing tumors where IPH4502 could be best in class versus other topo I Nectin-4 ADCs. With lacutamab, we are preparing for confirmatory study initiation in the second half of 2026 based on non-dilutive financing options, which are currently under negotiation with pharma partners and royalty structures. For monalizumab, the phase III PACIFIC-9 trial in non-small cell lung cancer has completed enrollment, with data expected for the primary endpoint in the second half of 2026. Taken together, these three programs provide a clear set of value-driving catalysts across our portfolio. Importantly, with a cash position of EUR 44.8 million at the end of 2025, we have funding visibility until the end of the third quarter of 2026, allowing us to continue executing on our key development priorities. Overall, we remain focused on advancing our pipeline and delivering on these upcoming milestones. With that, we're happy now to open for questions. We will now begin the question and answer session. If you would like to ask a question, please raise your hand now. If you have dialed in to today's call, please press star nine to raise your hand and star six to unmute. That is star nine to raise your hand and star six to unmute. Please stand by while we compile the Q&A roster. Your first question comes from the line of Swayampakula Ramakanth with H.C. Wainwright. Your line is now open. Please go ahead. Good morning or good afternoon, Jonathan and team. Thanks for doing this call. A couple of quick questions. Just to get started with IPH4502, you know, you are reporting some preliminary anti-tumor activity in the ongoing trial. You know, can you provide us some additional specifics regarding the program? And also, you know, with the changes going on within Nectin-4 ADCs, you know, among some of the competitors, you know, how do you see your program in terms of strength? And also, you know, how much outside interest is there for that specific program? Yeah. Maybe I can start off and address that, and maybe Sonia can hit some of the specifics, okay? I mean, we continue to be very excited by the IPH4502 program. Clearly the study is progressing very well, and there is a very significant amount of interest. We've been following the competitor activity here and what's been happening. If anything, we think that reinforces the competitive positioning of IPH4502. We're clearly focusing with the initial indication on the post-PADCEV setting. As a topo 1 ADC, we think we have a very good opportunity there, which was never open to MMAE-based ADCs. We think some of the recent developments are, will actually potentially help us and really show the clear differentiation in positioning that we have with IPH4502. Maybe, Sonia, you want to add something? Sure. We have established the MTD and this is going to be, let's say, at an expected level according to what we know for other exatecan-based assets. It is very encouraging to see this preliminary activity at the therapeutic dose in different tumor types. We're going to eventually explore even further this clinical activity. Okay. Thanks for that. On the MATISSE interim data presentation at AACR, you know, I'm glad that you got an oral presentation slot at the conference. You know, I'm not asking you to reveal the abstract or the details of the study, but in general, how should we think about the program itself and you know, what would we potentially be walking away from that oral presentation regarding that program? We're taking Yannis. Hi, R.K. Yannis Morel speaking. We are having this MATISSE clinical trial in collaboration with AstraZeneca, so Innate is running it. As you may remember, this program is under an option with AstraZeneca. Basically they, AZ has an opt-in point before starting any phase III. I would say my expectation is that this phase II is really dedicated to generate a sufficient data package to validate the target and to show if there is a path forward for the development in lung cancer. In terms of data, as you know, there is an embargo on the data until the meeting, as it is a clinical abstract. The design of the trial has been shown at the Trial in Progress poster at ESMO in 2023. It was disclosed at that point in time that there will be some interim analysis for efficacy. What will be presented at AACR is the interim on the first 40 patients, knowing that the trial is including up to 70 patients, and today the trial is continuing. Well, thank you for that, Yannis. Last question from me. You know, regarding the collaboration revenue from monalizumab program, you know, or, you know, in the recent filing, it looks like that it's dropped almost to zero at this point, having met all the obligations. Do you foresee any additional milestones, especially with the upcoming, you know, second half, PACIFIC-9 readout? With regards to revenue, you have to be careful because in fact it relates to the old agreement where we were co-developing the early stage of development. This is the very leftover, and those projects are over. Now the project is completely in the hand of AstraZeneca, so the accounting treatment is slightly different. It's not going through the revenue, it's through collaboration liability, so the balance sheet. You don't see it in revenue, it doesn't mean that we don't work actively together. The future development of the program will depend also on the upcoming results expecting on the second half of the year. Okay. Thank you. Thanks for taking all my questions. Your next question comes from the line of Daina Graybosch with Leerink Partners. Your line is now open. Please go ahead. Can you guys hear me? Can you hear me? Loud and clear. Sorry, I dialed in and it was a little confusing on Zoom. Thank you for the question. Another one on MATISSE going into the AACR presentation. If I recall, the initial data that Astra generated was in relapsed refractory lung cancer. I wonder if you could remind me of what you saw there with this program and why that gave Astra confidence to move this into the early stage setting. Hi, Daina. Yannis speaking. I think that one of the key takeaway from the phase I is that, if you may remember, we presented that at a poster at ESMO IO two years ago. Well, that we managed to identify a dose that was able to actually block the enzymatic activity in the patient of CD39. So as it was tested as a single agent and in combination with durvalumab in order to really define the dose to be explored in phase II. But what was really the key learning was that at the dose that we are using, we are really able, based on explants from patients, to block the pathway in the patients. That's why we are exploring this setting where there is also expression of CD39. It's something that again, we have published in a previous poster in this early lung cancer. It really gave us the opportunity to test the ability of by removing this adenosine pressure. We know that the antibody can do it. It's not the case of all the antibody that we have tested. We know that this one, IPH5201, can do it, to test whether it will translate into an increase of activity of durvalumab in setting where we know also based on the NeoCOAST trial, that durvalumab is active in this setting. Because maybe we haven't thought about CD39 in a while, can you just remind us how that fits in relation to CD73, which Astra has with oleclumab as another sub-study in PACIFIC-9? Just how they all fit together and whether CD39 alone is sufficient to block the adenosine inhibition. Inhibition. Yeah. Just to remind you, CD39 is the enzyme that is upstream in the pathway of degradation of ATP. ATP is sequentially degraded into ADP and then finally into adenosine, I would say, sequential degradation going through CD39 and then into CD73. CD73 is the downstream enzyme. By blocking CD73, you potentially decrease the quantity of adenosine within the tumor microenvironment, but you do not prevent the degradation of ATP. Whereas by blocking CD39, and it's something that we have published also in Cell Reports a few years ago, when you block CD39 upstream, you not only limit the accumulation of adenosine, but you also induce the accumulation of ATP, which is known to be immune-stimulating through the P2X receptor. It's something that we have shown in preclinical models that it's of particular interest, especially when you combine with an inducer of apoptosis like chemotherapy. That is also why it makes this neoadjuvant setting in the MATISSE trial so appealing because it's a combination of both with durvalumab, again, which is approved in this setting, in this perioperative setting in operable lung cancer, but also there is chemo, which is an important inducer of ATP that can be blocked and accumulated by the blockade of CD39. Thank you very much. Your next question comes from the line of Jeet Mukherjee with BTIG. Your line is now open. Please go ahead. Yes. Hi, can you hear me? We can hear you loud and clear, yes. Great. Thank you so much for taking the question. Maybe just starting with lacutamab, just any, color or updates you can share in terms of how those partnership discussions are going, and are there any particular, deal structures or outcomes that you feel best aligns with, Innate Pharma? I have a follow-up question. I think if we look at lacutamab and how we're moving forward, and I think this is alluding to the financing question, I think the most important thing here is that we get lacutamab on the market for patients in the fastest way possible. The timelines for approval from our perspective look similar for either a BD option or a royalty financing option. We also know that in either of those scenarios, we will be running the phase III studies. We will control the timelines and the regulatory interactions, and we'll be able to leverage our expertise and the networks that we've already established in CTCL. At the end of the day, our decision then is really based around what will bring the most value for shareholders in terms of the long-term value. That's what we're currently evaluating and looking at both the potential of the BD partnership or a royalty financing structure. Watch this space, and we should hopefully make a decision in the not too distant future. Great. Thanks for that. As my follow-up question, just coming back to IPH4502, in terms of the initial update that you'll disclose, is this one that'll come as perhaps, an investor webcast or perhaps at a medical conference? Are you able to say now if you've seen antitumor activity in other tumor types outside of urothelial carcinoma? Thank you. Maybe I can start off and then Sonia can give them the details. I mean, I think we're moving very well with this program. It's moving very fast. We have seen antitumor activity in both post-EV, but also in other tumor types. Maybe Sonia can fill us in on the details. I mean, of course, this is a work in progress, and, you know, it is always very difficult to say, be more specific on an ongoing trial. But definitely, yes, we had also some durable clinical activity in some individuals heavily pretreated. As Jonathan said, the data that we currently have show that our path forward in the EV, in the urothelial post EV may be plausible and supported by data. And also it was nice to see other clinical activity in other indication, and forgive me for not being too specific on this. We are aiming, of course, to present at a medical conference as soon as the data get mature, then we are obtaining all the, let's say, data around this phase I trial. Your next question comes from the line of Christopher Liu with Lucid Capital Markets. Your line is now open. Please go ahead. A reminder to unmute yourself locally when speaking. To unmute yourself, please press star six on your telephone keypad, or if using Zoom, just click on unmute. Hello. Can you guys hear me? hear you now, Christopher. Okay, perfect. Apologies. I disconnected before, so I had to rejoin the call. I apologize if I ask something that's already been asked. I just was wondering, you know, for the ADC, what can we expect to see from the upcoming data readouts? And then for lacutamab, what kind of sales infrastructure are you looking to build and, you know, how much are you looking to spend on something like that? You wanna take the first question, Sonia? In terms of study readout, what we are going to focus is to get the full safety profile. The PK that is also quite relevant in the ADCs and also show the level of free payload that may be of importance and influencing also the safety profile. Of course, all the efficacy readouts that we have from these patients, including the expression of Nectin-4 in their tumors because we collect tumor biopsies at screening to identify the expression of Nectin-4. This is done retrospectively and not prospectively in the study. We already know that some of the subjects we have enrolled had a negligible level of Nectin-4. This is done, of course, in batches. This is what we aim to have out of this phase I trial, and we intend to present to a medical conference. Addressing the second part of your question, Christopher, in terms of sales infrastructure. Just to reiterate that we've not made a decision yet whether we would do this ourselves or whether we would go through a potential B, BD partner. If we were to do this ourselves, what we have established is that CTCL, both mycosis fungoides is treated in a relatively small number of centers in the U.S. It's predominantly treated in academic centers. The majority of the patients are treated in 50 centers in the U.S., and pretty much all of the patients within 100 centers. You need a relatively small commercial infrastructure to be able to fully realize the associated commercial opportunity. Our estimate is a sales team, probably of around 20 people, a medical affairs team to support that of probably five or six people and a handful of access people. That's the sort of investment that you would actually be looking at if this was something that we ultimately decided to do ourselves. Got it. Thank you very much. There are no further questions at this time. I will now turn the call back to Jonathan Dickinson, CEO, for closing remarks. Okay. I'd like to thank everybody for attending the conference call today. Just to reiterate that it's an exciting year ahead for the company. We're very clearly on a path with lacutamab to initiating the phase III confirmatory study and unlocking the potential for the accelerated approval, a path to creating near-term revenue, which is important for Innate Pharma. With IPH4502, we're progressing very nicely, and we're expecting to approach some catalysts as we go through this year as we develop the dataset and develop a dataset that is robust and meaningful to patients, to shareholders, to investors, potential investors. Obviously that will generate some inflection points, which would allow us to look at in terms of how we could further fund that further development of IPH4502. Of course, finally, we have monalizumab, which is approaching a very important inflection point for the company. Thank you for your time and attention, and we look forward to interacting with you over the coming weeks and months. Thank you. This concludes today's call. Thank you for attending. You may now disconnect.