Operator
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 9 to raise your hand and star 6 to unmute. I will now hand the conference over to Stephanie Cornin, 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 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 programs, Laputamab, IPH 4502, and Monalizumab, as well as IPH 5201 in partnership with AstraZeneca. Speakers will be our CMO Sonia Quarattino, our COO Yanis Morel, and I. Frédéric Lombard, CFO, will comment 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 US 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 benefits. 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, lakutumab, and monolizumab. 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 ADC. 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 Telemat3 phase 3 trial with Locutumab 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 IPH 4502, our novel Nectin-4-ADC, where we see the potential to deliver a differentiated profile and address significant unmet needs across multiple tumor types. IPH 45-02 is progressing rapidly with early signs of anti-tumor activity in heavily pretreated patients, including in urophilial cancer previously treated with EV, and a favourable 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 urophileal cancer post-EV and selected additional tumor types and are excited by the progress we are seeing today. And third, monoluzumab, in partnership with AstraZeneca, represents an important late-stage asset with the Pacific 9 phase 3 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 lacutumab, our late stage asset in cutaneous tisal lymphoma. As a reminder, the phase 2 telomax study has demonstrated clinically meaningful and durable activity in both mucosus fungoidus and cesarean syndrome, including improvement in quality of life, with a favourable 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 incessary syndrome, as well as fast-track, crime and orphan drug designation. Second, these data support the potential accelerated approval path in Caesary syndrome, the most aggressive CTCL subtype, characterized by high-end medical need and no standard of care after treatment with Mogamulizumab. And lastly, we have received FDA clearance to proceed with the Telomac-3 study, which intends to be a confirmatory study for Caesaree syndrome and the registrational study for mycosis fungoidus. The initiation of Telomac-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 3 trial design. The proposed phase 3 study, Telomag3, is an open-label, multi-center, randomized comparative study to demonstrate the efficacy and safety of lacutamab in two separate cohorts of patients with cutaneous dysalymphoma 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 mogamolizumab, and patients will be randomized one-to-one to either lacutamab or romidepsin. In cohort two, patients with MF from stage 1b to stage four, who have failed at least one prior line of systemic therapy, will be randomized one-to-one to either lacutamab or mogamulizumab. Both cohorts will be randomized one-to-one and randomization will be stratified according to disease stage and region. The primary endpoint for both cohorts is PFS, bi-blinded independent central review. The secondary key endpoint for the SS cohort is overall survival, whilst the key secondary endpoint for mycosis fungoides are quality of life and pruritus. As the Caesary syndrome and mycosis fungoides studies subpopulation are considered as independent cohorts. Answering to distinct objectives, two sample sizes 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 as 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 3 initiation expected in the second half of 2026. Slide 11 outlines the projected regulatory timelines for lacutamab in cesarean syndrome and mycosis fungoides. As previously presented, the phase 2 telomac data in Caesary Syndrome are intended to support a potential accelerated approval once the confirmatory phase 3 trial is underway. In this context, the Telomac 3 study is designed to serve as a confirmatory trial for SS while also supporting full approval in mycosis fungoidus. In the MF cohort, the primary endpoint of progression-free survival is expected to support full approval in both US 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 and disindication. From a regulatory standpoint, this represents a statewide development approach, starting with caesaree 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 caesaree syndrome. Based on recent real-world data analysis, we estimate approximately 300 incident patients per year in Caesary 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, Caesary 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 Caesary 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 patients per year and the prevalence of around 12,000 patients in the US. Importantly, when looking at the current market, mugamulizumab generated approximately 300 million in annual sales in 2025 as planned and is projected to reach 350 350 million in 2026 with stronger adoption in cesary syndrome and more limited penetration in mycosis phongoides this provides a relevant benchmark for the market opportunity and highlights the potential for a therapy able to capture share across both caesary syndrome and mycosis mongroids. 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 cesare syndrome, expanding to over 500 million across cesare and mycosis pongoides in the second line setting, with additional upside as lacutamab moves into earlier line of therapy and broader patient segment over time. And with that, Yanis 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 Nectin4ADC 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 on the Nectin-4 target to a distant and non-offerlapping epitope versus N-forcumide. It is combined with a stable, cleavable, and hydrophilic linker which supports high systemic exposure of the ADC while minimizing the release of free exatican in the circulation and therefore reducing the risk of off-target toxicity. The payload, exatican, is a potent topoisomerase-1 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 anfortumab 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 first-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 feature. As you can see, the majority of Nectin-4 ADCs currently in clinical development, including approved and late-stage aid assets, are based on MME payloads such as importumabedotin or PADCELL. 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-1 payload, exatican, which we believe offers a differentiated mechanism of action. Importantly, this allows us to potentially overcome some of the limitations observed with MME-based conjugates, including activity in tumors that are resistant to or have progressed following N-fortumab vedotib. Indeed, MME-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 on fortumabedotin. In addition, as mentioned earlier, the strong bystander effect associated with exatican may enable activity in tumors with low or heterogeneous negative 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 topo-1-based N4-ADC. Turning to slide 16, here we present new preclinical data supporting the profile of IPH4502 as a potential best-in-class topo-1-N4-ADC. Starting on the left-hand side of the slide, in a CDX model with high N4 expression, IPH4502 demonstrates strong antitumor activity as other topo-1-ADC do. However, the key differentiation emerged in models with low NEC4 expression, where IPH4502 maintains meaningful anti-tumor activity, while other topo-1 ADC 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 observe a differentiated antitumor profile for IPHR4502, 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 epitome, a stable and hydrophilic linker, and a strong bystander effect of exatican. Now, handing over to Sonia, who will present you the IPH-45 Phase I trial.
Thank you. Now let's turn to slide 17. IPH-4502 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 bone designed 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 urotelial cancer, relapsed or refractory to unfortunate bedotin, 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 2 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 effect, 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. These 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. Second to Gera, this defines a clear therapeutic gap in the post-CV setting and IPH 4502 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 urotelial carcinoma, we are initially focusing on the post-EEB 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 IV-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 NEC4 expression. and overall our objective is to build a broad and modular clinical development strategy starting with high and met 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 Monalizumab and IPH5201. Starting with Monalizumab, the anti-NKG2A antibody co-developed with AstraZeneca, we remain focused on the progress of the phase 3 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 IX 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 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 2 studies in early lung cancer, including COST, NEO-COST and NEO-COST-2. PACIFIC-9 is a large global trial that has now completed enrollment with approximately 999 patients randomized in a 1 to 1, 1 ratio across the three treatment arms. The primary endpoint is progression-free survival with efficacy comparisons of both combinations versus Durvalobam 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 MATIS Phase II trial is a multi-center, 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 Nate 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 AECR 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 InAIDS. 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 of when Alizumab is approved, AstraZeneca will book sales and Innate Pharma will receive double-digit royalties on sales in the U.S. and the rest of the world. In Europe, as innate pharma is contributing to 30% of the funding for the phase 3 trials, we will get 50% of the profit and have the option to co-promote the drug. The agreement regarding IPH 5201 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 than the Monalizumab one, INATE has also the option to co-found phase 3 trials in order to get 50% of the profits in Europe and co-promotion rights. Otherwise, INATE Pharma will receive royalties in Europe like in the US and rest of the world. With that, I will now hand it over to Frédéric to walk you through the financial results.
Thank you, Yanis. So now turning to slide 25, I will walk you through our 2025 financial highlights. Revenue and other income amounted to 9 million this year. It includes 2.8 million from licensing and collaboration agreements, primarily related to recognition of proceeds from our partnerships with AstraZeneca and Sanatou, as well as 6.2 million in governmental funding for research expenditures. Operating expenses were $63 million, of which 73% were related to R&D. R&D expenses were $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 costs, partially offset by restructuring charges following the workforce restoring plan execution. G&E expenses were $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 impact. Turning to our cash position, we ended the year with $44.8 million in cash, cash equivalent, and financial assets as of December 31st, 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, Frederick.
And turning to the next slide. As we close, I would like to highlight the strength of our focus portfolio built around three high-value assets which are positioned to drive innate value. Starting with IPH 4502, we are making strong progress in phase one. The study is progressing very well with high interest, and we are enriching cohorts at the pharmacologically active dose levels. We have observed preliminary anti-tumor activity with a favorable safety profile to date, including in patients with urophilial 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-PADCEF 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 Locutumab, 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 monolizumab, the Phase III Pacific IX 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 $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.
Operator
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 start 9 to raise your hand and start 6 to unmute. That is start 9 to raise your hand and start 6 to unmute. Please stand by while we compile the Q&A roster. Your first question comes from the line of Swayan Pakula Ramankath with MHC Wang Wright. Your line is now open. Please go ahead.
Good morning or good afternoon, John. And team, thanks for doing this call. A couple of quick questions. You know, just to get started with IPH 4502, you know, you are, you know, reporting some preliminary anti, you know, tumor activity in the ongoing trial. You know, can you provide us some additional specifics regarding the program and also, you know, with 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, 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 IPH 4502 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 the IPH 4502. We're clearly focusing with the initial indication on the post-PADSF sitting and as a Topo 1 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 in positioning that we have with IPH 4502. Maybe Sonia, you want to add something?
Sure. We have established the NTD and this is going to be, let's say, at an expected level, according to what we know for other exotecan-based assets. And it is very encouraging to see this preliminary activity at the therapeutic dose in different tumor types. And we're going to eventually explore even further this clinical activity.
Okay. Thanks for that. And then on the MATIS interim data presentation at ASCR, you know, 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 So 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?
Hi, RK. So Yanis is speaking. So we are having this MATIS clinical trial in collaboration with AstraZeneca. So INAT is running it. As you may remember, this program is under an option with AstraZeneca. So basically, the AZ has an opt-in point before starting any phase three. I would say my expectation is that this phase two is really dedicated to generate a sufficient data package to validate the target and to show if there is a fast forward for the 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 has been shown at a trial-in-progress poster at ESMO in 2023. And it was disclosed at that point in time that there will be some interim analysis for efficacy. And what will be presented at ACR is the interim on the first 40 patients, knowing that the trial is including up to 70 patients, and today the trial is continuing.
Thank you for that, Giannis. Last question from me, you know, regarding the collaboration revenue from monolizumab program, you know, in the recent filing, it looks like it has 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. So this is the very leftover and those projects are over. So now the project is completely in the end 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. So you don't see it in revenue, doesn't mean that we don't work actively together. And the future development of the program will depend also on the upcoming results expecting in the second half of the year.
Thank you. Thanks for taking all my questions.
Operator
Your next question comes from the line of Dana Gray-Bosch with Lea Ring 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 us your confidence to move this into the early stage setting.
Yeah. Hi, Dana. Yanita speaking. I think that one of the key takeaways from the phase one is that, if you may remember, we presented that at a poster at ESMO IO a few years ago, was that we managed to identify a dose that was able to actually block the enzymatic activity in the patient of CD39. 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 two. But what was really the key learning was that at the dose that we are using, we are really able, based on explant from patients, to block the pathway in the patient. So that's why then we are exploring this setting where there is also expression of CD39. It's something that, again, was published in a previous poster in this early lung cancer. So 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 antibodies that we have tested. We know that this one, 5201, can do it to test whether it will translate into an increase of activity of durvalumab in a setting where we know also, based on the AJN trial, that durvalumab is active in this setting.
And then, 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 Oleclimab 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 so just to remind you cd39 is an 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
was i would say sequential degradation going through cd39 and then into cd73 so this is 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 and it's something that we have shown in pre-clinical model that it's of particular interest especially when you combine with a inducer of apoptosis like chemotherapy and that is also the why it makes this agent-like 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.
Operator
Your next question comes from the line of Yid Mukherjee with BTIG. Your line is now open. Please go ahead.
Yes. 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, you know, deal structures or outcomes that you feel best aligns with innate pharma?
And I have a follow up question. yeah so i i think if we look 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 uh lacutamab on the market for patients uh in in the fastest way possible uh and um the timelines for approval from our perspective look similar for either a bd option or a royalty multi-financing option. We also know that in either of those scenarios, we will be running the phase three studies. So we will control the timelines and the regulatory interactions, and we'll be able to, I guess, 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 the BD partnership or a royalty financing structure and watch this space and we should hopefully we should hopefully make a decision in the not-too-distant future.
Great. Thanks for that. And as my follow-up question, just coming back to 4502, in terms of the initial update that she'll disclose, is this one that'll come as perhaps an investor webcast or perhaps at a medical conference? And are you able to say now if you've seen anti-tumor activity in other tumor types outside of urethelial carcinoma?
Thank you. so maybe i can start off and then sonia can uh can can can give them the details i mean i i think we're moving very well with this program it's moving it's moving very fast um we have seen anti-tumor activity in both post ev but also in other tumor types and maybe sonia can fill us in on the details i mean of course this is a work in progress and And, you know, it is always very, 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 pre-treated. As Jonathan said, the data that we currently have show that our path forward in the urothelial post-EV may be plausible and supported by data. um 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 matured and we are obtaining all the let's say data around of
Operator
this phase one 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 hello can you guys hear me you know okay perfect uh apologies um i disconnected before so i had to rejoin the call so i apologize if i ask something that's already uh been asked but i just was wondering um you know for the adc what can we expect to see from the upcoming data readouts um 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 want to take the first question sony in terms of um 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. And of course, all the efficacy redoubts that we have from these patients, including the expression of Nectin-4 in their tumours, because we collect tumour biopsies at screening to identify the expression of Nectin-4. This is done retrospectively and not prospectively in the study. And so we already know that some of the subjects we have enrolled had a negligible level of Nectin-4. And this is done, of course, in batches. And so this is what we aim to have out of this phase one 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 cesare and mycosis fungoid, is treated in a relatively small number of centers in the US. It's predominantly treated in academic centers. The majority of the patients are treated in 50 centers in the US 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.
Got it. Thank you very much.
Operator
There are no further questions at this time. I will now turn a 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 three 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 IPH 4502, 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, potential investors. And 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 IPH 4502. And then, of course, finally, we have monoluzumab, 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.
Operator
This concludes today's call. Thank you for attending. You may now disconnect.
