Innate Pharma S.A. (NASDAQ:IPHA) Q2 2025 Earnings Call Transcript September 17, 2025
Innate Pharma S.A. beats earnings expectations. Reported EPS is $-0.2963, expectations were $-0.32845.
Operator: Thank you for standing by, and welcome to the Innate Pharma First Half 2025 Business Update and Financial Results Conference Call. [Operator Instructions]. I’d now like to turn the call over to Stéphanie Cornen, Vice President, Investor Relations and Communications. You may begin.
Stéphanie Cornen: Good morning and good afternoon, everyone. Thank you for joining us for Innate Pharma H1 2025 Business Update and Financial Results Conference Call. The press release and today’s presentation are both available on the IR section of our website. Before we begin, I’d 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’ll briefly cover today’s agenda. Our CEO, Jonathan Dickinson, will discuss our strategic overview, path forward and commercial opportunity. Our COO, Yannis Morel, will provide an update on the scientific differentiation of our lead ADC.
He will then hand over to our CMO, Sonia Quaratino, who will present clinical pipeline updates on IPH4502, lacutamab and monalizumab. Afterwards, our CFO, Frederic Lombard, will review the financials. Then Jonathan will return with closing remarks and we’ll open the call for Q&A. With that, I’ll now hand it over to Jonathan.
Jonathan Dickinson: Thank you, Stéphanie, and good morning to those joining from the U.S., and good afternoon to our participants in Europe. Moving to Slide 5. Innate Pharma’s foundation is in leveraging our deep scientific expertise to advance life-enhancing cancer therapies. Through our years of pioneering work in antibody engineering, we have built a differentiated high-value clinical pipeline supported by compelling data, and this positions us to deliver truly transformative treatments. Turning to Slide 6. During the first half of the year, we’ve made significant progress across our portfolio, and today marks an important new chapter for Innate. As you may have read in the press release for our half yearly update that we issued earlier today, we have made the strategic decision to focus our investment where we believe we can deliver the greatest impact for both patients and our shareholders.
Therefore, going forward, our main investments will be centered on 3 high-value clinical assets, IPH4502, lacutamab and monalizumab. These programs represent the strongest opportunities to transform care and create meaningful value, and they will form the focus of today’s discussion. At the same time, we will concentrate on selecting and advancing our next ADCs towards clinical development. As a consequence of this prioritization and sharpened focus, we intend to streamline our organization to deliver on our strategic objectives and key near-term milestones. This is a pivotal moment for Innate. We are aligning our strategy, our science, our organization and our investments to drive forward the programs that can truly make the biggest difference.
Q&A Session
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I could not be more confident in the path we are taking, and I’m excited to share with you how we will execute on this vision in the coming presentation. As you will also have seen in this morning’s announcement, our CSO, Eric Vivier, has decided to return to full-time academic research. Eric has been a true driver of the scientific agenda within Innate, so we are extremely pleased that he will continue to support the company’s innovation in the important role as an adviser to the R&D Committee of the Board of Directors. Our Chief Operating Officer, Yannis Morel, has always had responsibilities for preclinical research and development, and he will now also assume the Chief Scientific Officer responsibilities. With that, I will now hand it over to Yannis for a closer look at our lead ADCs and the potential.
Yannis.
Yannis Morel: Thank you, Jonathan. First, on Slide 8, let me share with you why we think Nectin-4 is an attractive target for a next-generation ADC and why our highly differentiated Nectin-4 ADC has more potential across many solid tumors. Even though Nectin-4 is a validated ADC target, PADCEV or enfortumab vedotin carries some challenges and has several limitations. It is approved solely for patients with urothelial cancer where Nectin-4 expression is the highest. In addition, PADCEV-related toxicity often leads to treatment discontinuations and relapse are frequently observed, creating a growing medical need in the post-PADCEV setting. Finally, even though Nectin-4 is expressed at moderate to high level in several other tumor types, there is limited evidence showing that PADCEV is active beyond urothelial cancer.
On the next slide, Slide 9. I want to show you why we are so excited by our next-generation Nectin-4 ADC program called IPH4502. As I said previously, this is a differentiated ADC that leverages a novel design to improve both safety and efficacy. IPH4502 is based on a proprietary humanized antibody that binds a unique epitope on the Nectin-4 molecule. The linker used is stable, cleavable and hydrophilic ensuring high ADC exposure and low systemic release of free exatecan, which minimize potential side effects. The payload itself, exatecan, is a potent topoisomerase I inhibitor. It shows what’s called bystander activity, which means it impacts number in tumor cells that do not express high level of Nectin-4 and can therefore address tumors with heterogenous expression of Nectin-4.
In addition, it remains highly active in enfortumab vedotin or MMAE-resistant models, allowing it to target tumors that have or became resistant to EV. In summary, the design of IPH4502 is purpose-built to overcome the limitations seen with existing therapies of [indiscernible] enfortumab vedotin. On the next slide, Slide 10, turning to preclinical data. During the period, we were also pleased to present at the AACR Annual Meeting, our filings, that highlights the differentiated potential of IPH4502. Starting from a PDX model of urothelial cancer, we generated a model of acquired resistance by exposing tumors to repeated cycle of enfortumab vedotin. As anticipated, tumors that were initially sensitive became resistant to EV, while keeping expression of Nectin-4.
But what is remarkable is that in the same model, IPH4502 maintained its activity. While EV lost efficacy, IPH4502 continued to control tumor growth, underscoring its differentiated profile and the opportunity to address patients who no longer responds to EV. On the next slide, Slide 11. Our preclinical data also demonstrated antitumor activity in PDX model with low or heterogenous Nectin-4 expression from various tumor types, including, for example, triple-negative breast, esophageal and head and neck cancers. These results highlight the potential of IPH4502 to extend the reach of Nectin-4 targeting beyond the urothelial cancer into tumor types with significant unmet medical needs. IPH4502 is currently in Phase I development, and we are very excited about the potential of this novel and differentiated Nectin-4 exatecan ADC to address high unmet medical needs both in bladder cancer post EV, but also in solid tumors with low or heterogenous expression of Nectin-4 representing a potentially broad market opportunity.
I’ll now hand over to Sonia, who will discuss the clinical progress of IPH4502 as well as our other clinical programs.
Sonia Quaratino: Thank you, Yannis. Today, I will focus on preclinical assets that represent the potential to create the highest value for Innate, IPH4502, lacutamab and monalizumab. In the next slide, starting with IPH4502, the ADC-directed against Nectin-4, this is a trial that is an asset that is currently investigated in a first-in-human Phase I study. Enrollment in this dose escalation is going very well, and we are now on track to complete enrollment before the end of Q1 2026. The objective of the study is to assess the safety, tolerability and preliminary efficacy of IPH4502 in advanced solid tumors known to express Nectin-4. And we are pleased to present this study in a trial-in-progress poster at ASCO Annual Meeting in Chicago last June.
The dose escalation is guided by an adaptive [indiscernible] design to determine the maximum tolerated dose. And once this is established, patients in 1 or 2 selected indications will be randomized across 2 dose levels to define the recommended Phase II dose as per FDA guidelines. The antitumor activity of IPH45 as a single agent will be further explored at RP2D in an expansion phase in selected indications in which signs of activities have been detected in the dose escalation, as well as confirming that the drug has a favorable safety profile and tolerability, the goal of this Phase I trial is to generate efficacy data that will guide the path forward for IPH4502, such as a basket trial in combination with standard of care or expansion phase to help maximize its value for both patients and shareholders.
In Slide 14, we have the key milestones ahead for IPH4502. With enrollment progressing well, we expect to report preliminary safety and activity data in the first half of 2026. The preclinical data presented earlier by Yannis, are guiding us towards 2 key hypothesis to be explored in the clinic. The first, it’s an urothelial carcinoma in the post EV setting, where IPH4502 may overcome resistance to EV. This represents an area of high unmet need with no approved drives and the potential to move rapidly into late-stage development is large. The second is to look for signals in other tumor types where a Nectin-4 expression may be low or heterogenous, which could open an even broader opportunity. With this hypothesis, the clinical data will guide us towards the indication where IPH4502 can make the greatest impact.
Now turning on next slide on lacutamab. We are close to completion of the Phase III protocol following alignment with the FDA and EMA. To recap, lacutamab is a first-in-class anti-KIR3DL2 antibody in development for the treatment of cutaneous T-cell lymphoma and peripheral T-cell lymphoma. In CTCL, lacutamab has already generated strong long-term follow-up data, which we presented at ASCO this year and which we will summarize in the next slide. Importantly, the regulatory pathway is clear, supported by key designations that position lacutamab for potential accelerated approval in Sézary syndrome. Our confidence in the program was further strengthened earlier this year when the FDA granted breakthrough therapy designation for relapsed or refractory Sézary syndrome based on the TELLOMAK Phase II results.
This designation is intended to accelerate both development and regulatory review of drugs that address serious conditions. Beyond CTCL, PTCL, peripheral T-cell lymphoma, represents a second indication. It’s a group of aggressive lymphomas with poor prognosis and a significant life cycle management opportunity for lacutamab. Importantly, KIR3DL2 correlates with worse clinical outcome. And is expressed in approximately 40% of PTCL patients. In PTCL, lacutamab has previously demonstrated some objective responses as a single agent, reinforcing the relevance of the target and providing the rationale to pursue development in combination with chemotherapy. Building on these findings, lacutamab is now being investigated in the KILT trial, a randomized Phase II in combination with gemcitabine and oxaliplatin versus gemcitabine and oxaliplatin in relapsed refractory KIR3DL2 positive PTCL patients.
When we move to next slide and to recap the data in CTCL that we presented at ASCO 2025, the long-term follow-up data from the TELLOMAK Phase II trial. Here, we see the results in Sézary syndrome, which is an aggressive subtype of CTCL and post mogamulizumab, where there are no approved drug, we have shown clinical efficacy. In heavily pretreated patients, all pretreated with Moga, lacutamab demonstrated a global overall response rate of 42.9%, and the medium progression-free survival of 8.3 months. Of note, the median duration of response was 25.6 months, underscoring lacutamab’s potential to deliver durable clinical benefit in this very aggressive and difficult to treat population. Turning in the next slide to mycosis fungoides. The long-term follow-up data from the TELLOMAK Phase II trial showed that lacutamab achieved a global overall response rate of 19.6%, with consistent activity observed regardless of KIR3DL2 expression level.
The median duration of response was 13.8 months and median progression-free survival was 10.2 months with no difference between the two sub groups. Importantly, in both Sézary syndrome and mycosis fungoides, every patient who achieved a complete response remained in response at the time of the data cutoff, once again highlighting lacutamab’s ability to deliver durable benefit even in heavily pretreated patients. In both indications, Sézary and mycosis fungoides, lacutamab was well tolerated with an excellent safety profile that supports its potential use for long systemic therapy. Now in the next slide, let’s look at the potential positioning of lacutamab in CTCL. The challenges in CTCL care are well known. The disease has a profound impact on quality of life with patients suffering from itching, fatigue and cutaneous lesions with important psychosocial implications.
Preventing progression to advanced stages is critical as outcome in Stage IIb and beyond are poor. Yet very few tolerable systemic options are currently available for early-stage patients. And this is where lacutamab can make a real difference. Our data have shown deep antitumor activity, durable responses and meaningful progression-free survival. Equally important, lacutamab has shown an excellent safety profile overcoming the tolerability concern of other systemic therapies in earlier stages of disease. Furthermore, lacutamab address the symptoms that matter most to patients with a positive impact on the quality of life. In the next slide, we see that the combination of strong efficacy with excellent safety makes lacutamab a unique candidate for earlier use of systemic therapy in CTCL.
And this becomes particularly important in mycosis fungoides, where survival estimates deteriorate once patients progress to more advanced stages. As you can see, in Stage IIb and beyond, the 5-year survival is lower than 50%. Poor survival in late-stage MF highlights the need for systemic therapies that can be used earlier to change the course of the disease. And here is where lacutamab could fill a critical gap offering a tolerable systemic option that can be introduced at an earlier time point with the potential to delay progression and improve patient outcomes. So altogether, we are on track to advance lacutamab towards Phase III in CTCL. As discussed, we are close to finalize the Phase III protocol following interaction with the FDA and EMA.
And once financing is secured, we will be positioning to initiate the confirmatory Phase III trial next year, with the potential for accelerated approval in the following year, and enrollment advances in Sézary syndrome targeting approximately 2027. The key next step will be to determine the optimal path forward whether through partnering or additional investor support, always with the goal of maximizing value for both patients and shareholders. In parallel, in PTCL, the LYSA-sponsored KILT trial continues to enroll patients. And we look forward to data from this study in 2026, which could further validate lacutamab’s potential across additional T-cell lymphoma. Now switching gear in the next slide. We discussed another late-stage program, monalizumab, with a great potential value creation for the company.
As a reminder, monalizumab is a first-in-class anti-NKG2A checkpoint inhibitor currently evaluated in Phase III clinical trial in lung cancer by our partner, AstraZeneca, in combination with durvalumab. Three Phase II trial, COAST, NeoCOAST and NeoCOAST-2, demonstrated a strong rationale for this combination in unresectable non-small cell lung cancer and in the neoadjuvant setting. Now the Phase III PACIFIC-9 trial aims to demonstrate efficacy of durvalumab in combination with either monalizumab or the AstraZeneca anti-CD73 antibody, oleclumab in patients with unresectable Stage III non-small cell lung cancer who have not progressed following classic platinum-based concurrent chemoradiation therapy. The study is now fully recruited, and it remains on track for primary completion at the end of the first half of 2026.
And this is an important catalyst for the program with data expected in the second half of 2026. Now I’m going to hand over to Jonathan again, who will walk through the commercial opportunity of these 2 late-stage assets, lacutamab and monalizumab.
Jonathan Dickinson: Thank you, Sonia, for showing how lacutamab has the potential to fundamentally reshape the care of CTCL patients. As you can see on Slide 23, the opportunity for lacutamab starts with Sézary syndrome, where following a potential accelerated approval in 2027, we see a clear launch pathway. In the past months, by assessing U.S. claims data, we have identified a significantly greater opportunity in Sézary syndrome than previously anticipated. It’s been established that there are around 1,000 Sézary syndrome patients in the U.S. with approximately 300 new cases each year and a large pool of post-mogamulizumab treated patients. This represents a meaningful and derisked first market opportunity for lacutamab following an accelerated approval.
After accelerated approval in Sézary syndrome, the opportunity expands into second-line plus setting for mycosis fungoides and ultimately, into earlier stages of CTCL patients, where a tolerable systemic option that are currently lacking and where lacutamab has the potential to create a new market opportunity and change the course of the disease for patients through early intervention to stop or delay disease progression beyond Stage IIa. It’s been established through the same U.S. claims data that there are approximately 20,000 CTCL patients in the U.S. with an incidence of approximately 5,000 patients suggesting a larger population than previously estimated based on publicly available data. These new dynamics, combined with the additional potential in PTCL have led us to reconsider our strategy and the value we assign to lacutamab.
To maximize the opportunity for lacutamab, we are currently planning to bring the product into Phase III and submit a BLA in Sézary syndrome, either with the support of investors or with a partner, but with improved deal terms. Already at launch, lacutamab has the potential to reach a substantial patient population, making it an interesting, profitable and value-creating opportunity for Innate Pharma. We are actively collecting additional CTCL market data and conducting further analysis, leveraging claims data and market research to further define the market opportunity. We plan to share the new data and market insights at the lacutamab-focused investor event by the end of the year. Turning now to Slide 24, and to monalizumab. Our partnership with AstraZeneca for monalizumab continues to represent a significant value driver for Innate.
The total agreement is worth up to $1.275 billion, and we have already received $450 million in upfront and milestone payments to date under this partnership. Moving forward, Innate is eligible to up to an additional $825 million in development and commercial milestones. Outside of Europe, AstraZeneca records all sales and Innate will receive double-digit royalties upon commercialization. In Europe, we retained co-promotion rights, along with a 50% profit share while contributing to a portion of the Phase III costs with a predefined cap. This structure ensures that Innate remains well positioned to benefit from monalizumab’s future success globally. That concludes the pipeline update for this presentation. I will now turn the floor to Frederic Lombard, our Chief Financial Officer, to discuss the financials for the first half of the year.
Frederic?
Frederic Lombard: Thank you, Jonathan. So for the first half of 2025, we’ve reported total revenue of EUR 4.9 million, primarily driven by collaborations with AstraZeneca and Sanofi as well as governmental funding for research expenditures. Operating expenses were reaching EUR 30.3 million with EUR 20.5 million in R&D and EUR 9.8 million in G&A expenses. R&D expenses decreased by 29% compared to the prior year, reflecting the phasing of certain clinical programs, while G&A expenses remained stable at EUR 9.8 million. At June 30, 2025, we had EUR 70.4 million in cash, cash equivalents and financial assets, providing a cash runway until the end of the third quarter of 2026. With that, I’m turning it back to Jonathan for closing remarks.
Jonathan Dickinson: Thank you, Frederic. Turning to Slide 28, you can see our news flow for the near and midterm, which is fully aligned with the strategic refocus I outlined at the beginning of today’s call. For IPH4502, our novel Nectin-4 ADC, the Phase I trial is progressing well and we expect data in the first half of 2026. While our preclinical R&D continues to build a strong ADC pipeline to fuel our next wave of candidates as shown by Yannis. Lacutamab has secured FDA breakthrough therapy designation, supported by long-term follow-up data presented at ASCO. And we are preparing the Phase III protocol submission following our discussion with regulators as indicated by Sonia. And for monalizumab, AstraZeneca’s Phase III PACIFIC-9 trial is fully recruited and remains on track for primary completion in the first half of 2026 with data expected in the second half of 2026.
Turning to Slide 29. In summary, we are excited about the opportunities ahead and confident in our ability to deliver value for patients and shareholders. We are concentrating our investment on what we believe are our highest value clinical stage assets, IPH4502, lacutamab and monalizumab, where we have multiple near-term catalysts, and we will rightsize our organization to deliver on these strategic priorities. With EUR 70.4 million in cash at the end of June, we are funded to the end of the third quarter of 2026, providing Innate the ability to execute on our focused strategic priorities. Thank you for your attention. And with that, operator, please open the line for questions.
Operator: [Operator Instructions] Your first phone question today comes from the line of Daina Graybosch from Leerink Partners.
Bill Ling: You got Bill on for Daina. So I guess, what should we take away on the potential of targeting NK cells now that ANKET’s are not included in your prioritization today as well as Eric Vivier sort of leaving the company?
Jonathan Dickinson: So takeaways from — I would like to say from Eric leaving the company, maybe that’s the place to start off. Eric is leaving the company, but he will still play an important role with the company moving forward. He will be an adviser to the R&D Committee of our Board of Directors. And we have an extended research collaboration with his lab. So we basically will continue to benefit from any innovation, which Eric can bring to the table. Moving back to NK cells and the reading, we are still working on NK cells. It’s not our main priority today. We’re focusing on what we believe are our highest value clinical assets, IPH4502, lacutamab and monalizumab. We will be basing all future decisions on our NK cell engagers on clinical data and the relevance of that clinical data to markets, and we’ll make the appropriate decisions on those assets when we have that clinical data and establish market relevance based on that data.
So it’s not the end of NK cells, but it’s not our priority today anymore.
Operator: We’ll move on to our next question, and it comes from the line of Swayampakula Ramakanth from HCW.
Swayampakula Ramakanth: So now that the ANKET programs are out at least as far as your development is concerned. Any commentary on where Sanofi is with the assets that they currently are developing?
Jonathan Dickinson: Absolutely. So I’d just like to say that it’s not the end of the story for NK cells. We’re still moving forward and completing the studies with IPH6501. We have a path to explore IPH61 via investigator-initiated research and an interesting way forward. So I wouldn’t say it’s the end of NK cells. It’s just that it’s been basically lowered in our current company priorities. From a Sanofi perspective, Sanofi continues to progress the BCMA-targeted ANKET. And as I think we’ve communicated in the past, that’s being explored in autoimmunity, in immunology as part of Sanofi’s focus as a company, and we expect to have updates from Sanofi on that BCMA program in the near future.
Swayampakula Ramakanth: And then regarding the Phase III start for lacutamab, should we still assume that unless you have a partner signed up ahead of the start of the study, it will still — it will be a wait and watch until you get a partner or you have enough commitment from investors to go ahead and start that study?
Jonathan Dickinson: So we are actively working with investors at the moment to basically keep options open. So we’re continuing discussions with partners, but we also have some very advanced discussions with investors who are very interested in lacutamab, now that we effectively have a derisked development program to move forward into Phase III. And we also see interest based now on the increased potential commercial opportunity. This also will reinvigorate discussions with partners. And we are also expecting next steps with respect to the finalization of the protocol for the confirmatory Phase III study, which is also an important step for partners. So we continue the discussions with partners. But at this stage, we see it as very important to keep our future options open to either go down the partner route, but with improved deal terms based on the significantly larger potential market opportunity, particularly with the first accelerated approval launch in Sézary syndrome.
And so yes, we’re keeping the options open with both — for both moving forward with investors and with potential partners.
Swayampakula Ramakanth: So last question from me, Jonathan. This is on 4502. Based on the preclinical data that you have generated so far, what potential indications do you think 4502 will be effective? And since there are numerous Nectin-4 ADC’s in the clinic right now, how differentiated are you is 4502 against those?
Jonathan Dickinson: Yes. So maybe, Sonia, you can take the first part of that question, Sonia?
Sonia Quaratino: Yes. Can you repeat the question, please?
Swayampakula Ramakanth: Yes. Based on the preclinical data that you have generated to date, what indication do you think is where 4502 could be effective?
Sonia Quaratino: Right. As I mentioned before, we focus on any indication that express Nectin-4 because we believe that we also can target dose indication with a relatively small Nectin-4 expression, but we also very much focus on the urothelial cancer patients who became refractory or resistance to PADCEV. And for these patients, there are no approved drugs. And if we have clinical — good clinical data in this refractory relapsed patients, we really may have a very fast opportunity for an accelerated market approval in UC post-PADCEV. So we are exploring, let’s say, the classic path as well as some more defined area for an accelerated — potential accelerated approval.
Jonathan Dickinson: And then in terms of differentiation, RK, I mean, I think we believe that we’ll be able to show differentiation here, particularly versus PADCEV or MMAE-based ADCs, due to the payload and the different resistance and toxicity profile, which we believe we’ll be able to show meaningful differences between IPH4502 and MMAE-based ADCs.
Operator: Your next question comes from the line of Justin Zelin from BTIG.
Justin Zelin: Maybe I’ll continue the questioning on 4502. If you can just give us an update on how enrollment has been progressing here. I know you gave an update here on enrollment completion. Just was curious on how you could comment on how enrollment is going today. When we should expect the initial data, if it will be sometime in the first half of next year, how many patients’ worth of data we should expect? And any expectations from a safety or efficacy standpoint from that update?
Jonathan Dickinson: Sonia, do you want to take that one?
Sonia Quaratino: Of course, of course. As mentioned, the enrollment with IPH45 is going extremely well. We always have, let’s say, a list of patients to go in — at a different dose level. And also with the [indiscernible] design that we have, we also have the possibility to have parallel enrollment in backfill cohorts. And so, we do not have the classic 3 plus 3 design with an extremely limited number of patients, but we can expand different to dose levels as we go along. To your question, of course, we plan to finish the enrollment in the first quarter of 2026. And of course, the data in terms of at least from the first CT scan can only occur as you can understand, 8 weeks later from the first dosing, so it takes another quarter to have the clinical efficacy from the last cohort recruited. Having said that, we are going to have probably a pool of data of 50, 60 patients by then.
Operator: And there are no further phone questions at this time. I will now turn the call back over to management for any written questions.
Stéphanie Cornen: Yes, we have one question on the line here from Rajan Sharma. So the first question is, does the new strategic focus means, ANKET assets will not be progressed irrespective of clinical data, given that 6501 data are expected in the near term?
Jonathan Dickinson: So, I think I answered this earlier, but I’ll repeat it again. So from an IPH6501 perspective, the study continues, and we expect to have data, I think, as we’ve communicated previously, towards the end of this year or very early next year. And we will make any decisions on the next steps for IPH6501 based on that clinical data and the clinical relevance of that data to the marketplace.
Stéphanie Cornen: Okay. And so the next question, what is the financial impact of the strategic refocus and head count reduction and what proportion of current R&D expense are directed towards IPH4502 and lacutamab?
Jonathan Dickinson: So the financial impact, we’ve not — and we won’t be communicating specific numbers on the impact of the financial reductions. We’re in a legal process now, which is a French legal process to reduce the size of the organization, which gives us an obligation not to communicate on certain components, and that would fall under that legal framework that we’re operating within. So we can’t provide specific guidance there. In terms of R&D expenses, maybe Frederic would like to comment on the proportion.
Stéphanie Cornen: So the question was, what proportion of current R&D expenses are directed towards IPH4502 and lacutamab?
Frederic Lombard: Yes, we usually never communicate on the investment that we do in those 2 in the portfolio. But following up on the comment from Jonathan, we have a significant portion of our external expenditure, which are on those assets.
Stéphanie Cornen: So we have another question from Oussema Denguir. So with regard to financial visibility, does estimate for the end of the third quarter of 2026, taking into account the impact of the restructuring plan?
Jonathan Dickinson: The answer to that is yes. So the restructuring plan is fully embedded into the cash runway, which takes us to the end of Q3 2026.
Stéphanie Cornen: And last question, concerning Phase III of lacutamab, can you provide an initial estimate of the investment requirements, if you decide to trial without a partner?
Jonathan Dickinson: Again, this is something that we would not normally communicate on in terms of the cost. This is a standard Phase III study. So I think you can draw your own conclusions. It’s nothing too dissimilar from similar oncology Phase III trials.
Stéphanie Cornen: Thank you, Jonathan. There is no further question.
Jonathan Dickinson: Okay. So thank you for everybody’s time and attention and for your interest in Innate Pharma, and we’ll look forward to meeting with you in person in the near future or on one of our next calls. Thank you, and goodbye.
Operator: This concludes today’s conference call. Thank you for your participation. You may now disconnect.
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