Ladies and gentlemen, thank you for joining us, and welcome to the Innate Pharma Full Year 2025 Earnings Call. I will now hand the conference over to Stephanie Cornen, Vice President of Investor Relations, Communications and Commercial Strategy at Innate Pharma. Please, Stephanie, 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 expectations. These statements involve risks 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 programs, 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. Frederic Lombard, CFO, will comment on our financial results. Jonathan will return with upcoming catalysts and closing remarks before we open the call for Q&A. With that, I'll now hand it over to Jonathan.

Thank you, Stephanie. Good morning to those joining from the U.S., and good afternoon to our European audience. Turning to Slide 5. 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 6. 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 7. 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 are 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 enfortumab vedotin, 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 enfortumab vedotin, and selected additional tumor types and are excited by the progress we are seeing to date. And 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 9 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 Sezary 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 Sezary syndrome as well as Fast Track, PRIME and Orphan Drug Designation. Second, this data supports a potential accelerated approval path in Sezary syndrome, the most aggressive CTCL subtype characterized by high unmet medical need and no standard of care after treatment with mogamulizumab. And lastly, we have received FDA clearance to proceed with the TELLOMAK-3 study, which intends to be a confirmatory study for Sezary 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 1, there will be patients with any stage Sezary syndrome who have failed at least one prior line of systemic therapy, including mogamulizumab, and patients will be randomized 1:1 to either lacutamab or romidepsin. In Cohort 2, patients with Mycosis Fungoides from Stage 1b to Stage 4 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 progression-free survival by blinded independent central review. The secondary key endpoint for the Sezary syndrome cohort is overall survival, while the key secondary endpoints for Mycosis Fungoides are quality of life and pruritus. As the Sezary syndrome and Mycosis Fungoides study subpopulations are considered independent cohorts with distinct objectives, two sample sizes are estimated to meet the primary endpoint in both Sezary syndrome and Mycosis Fungoides cohorts independently. As such, the study is powered to demonstrate superiority of lacutamab effect on PFS as compared to romidepsin in patients with Sezary syndrome who received at least one prior line of systemic therapy, including mogamulizumab, and compared to mogamulizumab in patients with Mycosis Fungoides 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 Sezary syndrome and Mycosis Fungoides. As previously presented, the Phase II TELLOMAK data in Sezary 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 Sezary syndrome while also supporting full approval in Mycosis Fungoides. In the Mycosis Fungoides 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 represents a stepwise development approach, starting with Sezary syndrome with the highest medical need and then expanding into the broader CTCL population.

From a commercial perspective, we see a focused and attractive opportunity for lacutamab in CTCL starting with Sezary syndrome. Based on recent real-world data analysis, we estimate approximately 300 incident patients per year in Sezary 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 enables a targeted commercial approach with limited infrastructure. At the same time, Sezary 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 Sezary syndrome is not a stand-alone opportunity, but a direct entry point into the broader CTCL market. Mycosis Fungoides represents a significantly larger opportunity with approximately 3,000 incident patients per year and a prevalence of around 12,000 patients 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 Sezary syndrome and more limited penetration in Mycosis Fungoides. This provides a relevant benchmark for the market opportunity and highlights the potential for a therapy able to capture share across both Sezary syndrome and Mycosis Fungoides. From a value perspective, the key drivers 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 $150 million in Sezary syndrome expanding to over $500 million across Sezary syndrome and Mycosis Fungoides in the second-line setting with additional upside as lacutamab moves into earlier line of therapy and broader patient segments over time. And with that, Yannis and Sonia will now walk you through IPH4502.

Thank you, Stephanie. 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 binds the Nectin-4 target to a distant and non-overlapping epitope versus enfortumab vedotin. 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 highlight its key differentiating features. 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 mechanisms. In contrast, IPH4502 is based on a TOPO1 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 settings 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 compelling mechanism, positioning it as a potential best-in-class TOPO1-based Nectin-4 ADC. Turning to Slide 16. Here, we present new preclinical data supporting the profile of IPH4502 as a potential best-in-class TOPO1 Nectin-4 ADC. Starting on the left-hand side of the slide, in a CDX model with high Nectin-4 expression, IPH4502 demonstrates strong antitumor activity as other TOPO1 ADCs do. However, the key differentiation emerged in models with low Nectin-4 expression where IPH4502 maintains meaningful antitumor activity while other TOPO1 ADCs in clinical development show a clear loss of efficacy. This is particularly important as it highlights the unique ability of IPH4502 to remain active in tumors with lower target expression. Overall, across multiple in vivo models, we consistently observed a differentiated antitumor profile for IPH4502, supporting its potential as a 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 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 tumors 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 being explored, and we are enriching cohorts 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 urothelial carcinoma models resistant to enfortumab vedotin, we are focusing on patients with urothelial carcinoma who progressed after enfortumab vedotin treatment. Despite the significant progress enfortumab vedotin 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 progressed 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 options for these patients 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 to five months and an overall survival in the range of seven to eight months with chemotherapy-based regimens. Taken together, this defines a clear therapeutic gap in the post-enfortumab vedotin 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-enfortumab vedotin 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 who progress after enfortumab vedotin-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. And overall, our objective is to build a broad and modular clinical development strategy, starting with high unmet need populations and expanding into earlier lines of therapy and additional tumor types over time, depending on the emerging data. Slide 20, I will now turn to monalizumab 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 represents the next key step in the development of monalizumab. In 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, compared to durvalumab alone in patients with unresectable 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 on 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 preplanned 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 to up to $1.275 billion of milestones. We already received $450 million and remain eligible to additional $825 million of potential payments. In the case monalizumab is approved, AstraZeneca will book sales and Innate Pharma will receive double-digit royalties on sales in the 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 to $825 million. This agreement, having a similar structure to the monalizumab one, gives Innate 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 as in the U.S. and rest of the world. With that, I will now hand it over to Frederic to walk you through the financial results.

Thank you, Yannis. So 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 studies' maturity as well as a decrease in indirect R&D expenses, primarily due to lower staff costs and reduced scientific consulting and IP costs, partially offset by restructuring charges following the workforce restructuring plan execution. G&A expenses were EUR 19.4 million, broadly stable year-on-year with a decrease in nonscientific consulting fees and reduced insurance expenses, partially offset by the workforce restructuring plan impact. Turning to our cash position. We ended the year with EUR 44.8 million in cash, 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, Frederic, and 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, who are relapsed or refractory to enfortumab vedotin, 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 TOPO1 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. And 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.

Your first question comes from Swayampakula Ramakanth of H.C. Wainwright.

A couple of quick questions. Just to get started with IPH4502, you were reporting some preliminary antitumor activity in the ongoing trial. Can you provide us some additional specifics regarding the program? And also with changes going on within Nectin-4 ADCs among some of the competitors, how do you see your program in terms of strength and also how much outside interest is there for that specific program?

Yes. So maybe I can start off and address that, and maybe Sonia can hit some of the specifics, RK. So 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. And as a TOPO1 ADC, we think we have a very good opportunity there, which was never open to MMAE-based ADCs. So we think some of the recent developments will actually potentially help us and really show the clear differentiation and positioning that we have with IPH4502. And maybe, Sonia, you want to add something?

Sure. We have established the MTD, and this is going to be at an expected level according to what we know for other exatecan-based assets. And it is very encouraging to see this preliminary activity at the therapeutic dose in different tumor types. And we are going to eventually explore even further this clinical activity.

Okay. And then on the MATISSE interim data presentation at AACR, I'm glad that you got an oral presentation slot at the conference. 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 what would we potentially be walking away from that oral presentation regarding that program?

You are taking it Yannis?

Yes. RK, Yannis speaking. So 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. So basically, AstraZeneca has an opt-in point before starting any Phase III. 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 development in lung cancer. And 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 was shown at the trial-in-progress poster at ESMO in '23. It was disclosed at that point in time that there would be some interim analyses for efficacy. And what will be presented at AACR is the interim on the first 40 patients, knowing that the trial includes up to 70 patients. And today, the trial is continuing.

Last question from me regarding the collaboration revenue from the monalizumab program in the recent filing, it looks like that's dropped almost to zero at this point, having met all the obligations. Do you foresee any additional milestones, especially with the upcoming second half PACIFIC-9 readout?

With regards to the 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. So this is the very leftover, and those projects are over. So now the project is completely in the hands of AstraZeneca. So the accounting treatment is slightly different. It's not going through the revenue, it's through collaboration liabilities on the balance sheet. So you don't see it in revenue. It doesn't mean that we don't work actively together. And the future development of the program will depend also on the upcoming results expected in the second half of the year.

Your next question comes from the line of Daina Graybosch with Leerink Partners.

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?

Daina, Yannis speaking. I think that's one of the key takeaways from Phase I is that, if you may remember, we presented that at a poster at ESMO IO a few years ago. We managed to identify a dose that was able to actually block the enzymatic activity of CD39 in patients. So 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. So that's why then 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 early lung cancer. So it really gives us the opportunity to test the ability of removing this adenosine pressure. We know that the antibody can do it. It's not the case of all the antibodies 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 the setting where we also know based on the PACIFIC trial that durvalumab is active in this setting.

And then 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 substudy in PACIFIC-9. Just how they all fit together and whether CD39 alone is sufficient to block the adenosine inhibition?

Yes. So just to remind you, CD39 is the enzyme that is upstream in the pathway of degradation of ATP. So ATP is sequentially degraded into ADP and then finally into adenosine via sequential degradation going through CD39 and then into CD73. So CD73 is the downstream enzyme. So 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 inducers of apoptosis like chemotherapy. And that is also why this agent and setting in the MATISSE trial is so appealing because it's a combination of both with durvalumab, again, which is approved in this perioperative setting in unresectable lung cancer, but also there is chemotherapy, which is an important inducer of ATP that can be accumulated by the blockade of CD39.

Your next question comes from the line of Jeet Mukherjee with BTIG.

Great. Maybe just starting with lacutamab. 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 align with Innate Pharma? I have a follow-up question.

Yes. So I think if we're looking 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. And the timelines for approval from our perspective look similar for either a business development option or a royalty financing option. We also know that in either of those scenarios, we will be running the Phase III studies. So 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. So 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. And that's what we're currently evaluating and looking at both the potential of a BD partnership or a royalty financing structure. Watch this space, and we should hopefully make a decision in the not-too-distant future.

Great. And as my follow-up question, just coming back to IPH4502, in terms of the initial update that you'll disclose, is this one that will come as perhaps an investor webcast or perhaps at a medical conference? And are you able to say now if you've seen antitumor activity in other tumor types outside of urothelial carcinoma?

So maybe I can start off and then Sonia can give the details. I think we're moving very well with this program. It's moving very fast. We have seen antitumor activity in both post-enfortumab vedotin, but also in other tumor types. And maybe Sonia can fill in on the details.

Of course, this is a work in progress. And it is always very difficult to be more specific on an ongoing trial. But definitely, yes, we have had some durable clinical activity in some individuals who are heavily pretreated. As Jonathan said, the data that we currently have show that our path forward in the post-enfortumab vedotin urothelial setting may be plausible and is supported by data. Also, it was encouraging to see clinical activity in other indications. 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 mature and we have obtained all the data around this Phase I trial.

Your next question comes from the line of Christopher Liu with Lucid Capital Markets.

Apologies. I disconnected before, so I had to rejoin the call. So I apologize if I ask something that's already been asked. But I was wondering 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 how much are you looking to spend on something like that?

Take the first question, Sonia?

In terms of the study readout, what we are going to focus on is to get the full safety profile, the PK, which is also quite relevant in ADCs, and also show the level of free payload that may be of importance and influence the safety profile. And 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 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 in batches. So this is what we aim to have out of this Phase I trial, and we intend to present to a medical conference.

And then 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 BD partner. If we were to do this ourselves, what we have established is that CTCL, both Sezary syndrome and 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. So as you can imagine, you need a relatively small commercial infrastructure to be able to fully realize the associated commercial opportunity. So 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. So that's the sort of investment that you would actually be looking at if this was something that we ultimately decided to do ourselves.

There are no further questions at this time. I will now turn the call back to Jonathan Dickinson, CEO, for closing remarks.

Okay. So I'd like to thank everybody for attending the conference call today. And 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 and then a path to creating near-term revenue, which is important for Innate Pharma. Then 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 data set and develop a data set that is robust and meaningful to patients, to shareholders, to investors and potential partners. That will generate some inflection points, which would allow us to look at how we could further fund the development of IPH4502. And then, of course, finally, we have monalizumab, which is approaching a very important inflection point for the company. So 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.