Good morning and good afternoon, everyone. Thank you for joining us for Innate Pharma's Q1 2026 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 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. To briefly cover today's agenda, our CEO, Jonathan Dickinson, will begin with a strategic overview and outlook.

Sonia Quaratino, our Chief Medical Officer, and Yannis Morel, our Chief Operating Officer, and I will then provide updates on lacutamab, IPH4502, and next-generation ADCs, as well as AstraZeneca-partnered programs, including monalizumab and IPH5201. Jonathan will then return with closing remarks.

Frédéric Lombard, our CFO, will join us for the Q&A. With that, I will now hand it over to Jonathan.

Thank you, Stéphanie. Good morning to those joining from the US, and good afternoon to our European participants.

Turning to slide 5, we continue to execute against our strategy, which is focused on our three priority assets, with discipline, and we're pleased with the strong progress we are seeing today. Starting with lacutamab, our anti-KIR3DL2 monoclonal antibody, which is being developed in cutaneous T-cell lymphoma, or CTCL.

As you remember, we received the FDA clearance to proceed with the TELLOMAK-3 Phase 3 trial for lacutamab in CTCL, and we expect to be able to initiate the study in the second half of 2026. We have made progress in negotiating non-dilutive financing options for lacutamab, including potential pharma partnerships and royalty-based structures.

From a commercial perspective, we believe that lacutamab represents a meaningful opportunity in CTCL in both the United States and Europe, with additional lifecycle expansion opportunities in peripheral T-cell lymphoma. Moving to IPH4502, our differentiated Nectin-4 ADC, which is being evaluated in advanced solid tumors.

The Phase 1 study is ongoing and approaching completion of enrollment in the dose-escalation phase and backfill cohorts. As highlighted on the slide, we continue to observe preliminary antitumor activity in heavily pretreated patients, including in urothelial cancer patients previously treated with EV.

We believe that IPH4502 may represent a differentiated opportunity, both in the post-Padcev urothelial cancer setting and, potentially, across a broader range of solid tumors. Finally, turning to monalizumab, our AstraZeneca-partnered anti-NKG2A monoclonal antibody, which is being developed in non-small cell lung cancer.

The ongoing PACIFIC-9 Phase 3 study remains on track for a planned readout in the second half of 2026. From a financial perspective, the partnership also continues to represent a potentially important source of future value for Innate, including potential milestones, profit sharing in Europe, and royalties in the United States and the rest of the world.

Overall, we believe these three assets provide Innate with a focused portfolio of differentiated clinical-stage opportunities, spanning both proprietary and partnered programs. I'll now hand over to Sonia and Stéphanie for a more detailed review of the lacutamab program.

Thank you, Jonathan. Turning to slide 7, lacutamab continues to progress towards initiation of the TELLOMAK-3 confirmatory Phase 3 trial and the potential accelerated approval pathway in Sézary syndrome.

As a reminder, the Phase 2 TELLOMAK study has demonstrated clinically meaningful and durable activity in both mycosis fungoides and Sézary syndrome, including improvement in quality of life, with a favorable safety and tolerability profile, supporting potential for long-term treatment. Based on these data, lacutamab has received Breakthrough Therapy Designation from the FDA in relapsed or refractory Sézary syndrome.

It has previously received Fast Track designation from the FDA, PRIME designation from EMA, and Orphan Drug status in both the United States and Europe. The Phase 2 data from the TELLOMAK trial also support the potential accelerated approval filing in Sézary syndrome once the confirmatory Phase 3 trial is underway.

In the next slide, the planned 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, patients with any stage Sézary syndrome who have failed at least one prior line of systemic therapy, including mogamulizumab, will be randomized 1:1 to either lacutamab or romidepsin.

In cohort 2, patients with MF, ranging from stage 1B to 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 the cohorts is progression-free survival assessed by blinded independent central review. The secondary endpoint for the Sézary cohort is overall survival, while the key secondary endpoints for the MF cohort are quality of life and pruritus.

The TELLOMAK-3 study is designed to serve as the confirmatory trial for Sézary syndrome, while also supporting full approval in mycosis fungoides. From a regulatory standpoint, we have received FDA clearance to proceed with this clinical trial protocol, and we continue towards Phase 3 initiation, expected in the second half of 2026.

Stéphanie will now go through the commercial opportunity. Stephanie Cochennec (Vice President of Investor Relations, Communication, and Commercial Strategy):

Thank you, Sonia. We continue to believe lacutamab represents an attractive commercial opportunity, supported by a focused and efficient commercial footprint.

Starting with Sézary syndrome, based on recent real-world data analysis, we estimate approximately 300 incident patients per year in Sézary syndrome in the US, with a prevalence of around 1,000 patients, the majority of whom are treated in a limited number of specialized academic centers. 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 US.

These data, from an analysis conducted by ZS Associates, are now available in the EHA 2026 online abstract book. This is a highly concentrated treatment landscape, with over 85% of patients managed in academic centers, and a large proportion treated within approximately 50 key institutions.

This concentration enables a targeted commercial approach with limited infrastructure. At the same time, Sézary syndrome and mycosis fungoides share the same prescriber base, which is a critical point from a commercial perspective.

This means that an initial launch in Sézary syndrome is not a standalone opportunity, but a direct entry point into the broader CTCL market. Importantly, when looking at the current market, mogamulizumab generated approximately $300 million in annual sales in 2025, as planned, and is projected to reach $350 million in 2026, with strong adoption in Sézary syndrome, and more limited penetration in mycosis fungoides.

This provides a relevant benchmark for the market opportunity, and highlights the potential for a therapy able to capture share across both Sézary syndrome and mycosis fungoides. From a value perspective, key drivers include treatment duration, which is supported by durability of responses, pricing, and market share across a broader eligible patient population.

Taken together, these support a stepwise commercial strategy, starting with an initial opportunity of up to $150 million in Sézary syndrome, expanding to over $500 million across Sézary syndrome and mycosis fungoides in the second-line setting, with additional upside as lacutamab moves into earlier lines of therapy and broader patient segments over time. I will now hand it over to Yannis to start the update on IPH4502.

Thank you, Stéphanie. IPH4502 is our novel and differentiated Nectin-4 exatecan ADC, which is in Phase 1.

Turning to slide 11, IPH4502 has been designed to overcome the limitation of the first-generation Nectin-4 ADCs and to deliver a more favorable therapeutic profile across multiple solid tumors. The drug candidate is based on a proprietary humanized antibody that binds to a distinct, non-overlapping epitope versus enfortumab on the Nectin-4 target.

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 circulation, and therefore reducing the risk of off-target toxicity. The payload, exatecan, is a potent topoisomerase 1 inhibitor with strong bystander activity, enabling to target not only Nectin-4-expressing tumor cells, but also neighboring cells with lower or heterogeneous expression.

Moreover, it is not sensitive to the mechanism of drug resistance related to MMAE, allowing to address patients who have been pre-exposed to Padcev. Next slide shows how IPH4502 is positioned within the evolving Nectin-4 ADC landscape.

The first wave of Nectin-4 ADCs largely relied on the MMAE payloads, including enfortumab vedotin. While EV has validated Nectin-4 as an important ADC target, other MMAE-based approaches will most likely face similar limitation than EV, such as MDR1-mediated resistance and peripheral neuropathy.

IPH4502 is designed to address these limitations through its topoisomerase payload and differentiated linker design. We believe this create a potential opportunity in bladder cancer, particularly in the post-enfortumab vedotin setting, as well as across multiple tumor types with low or moderate Nectin-4 expression.

Overall, we believe IPH4502 has the potential to be best-in-class topo 1 Nectin-4 ADC, driven by its differentiated design. On the next slide, we show newly generated preclinical data that continue to reinforce the best-in-class potential of IPH4502 as a topo 1 Nectin-4 ADC.

You can see that in both high and low Nectin-4-expressing models, IPH4502 demonstrates robust antitumor activity. However, the key differentiation versus other topo 1 Nectin-4 clinical ADCs appears in models with low Nectin-4 expression.

IPH4502 maintains meaningful antitumor efficacy, while the other clinical ADCs show a clear loss of activity. This is really 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 better efficacy for IPH4502, supporting its best-in-class agent potential, particularly in low to moderate Nectin-4-expressing tumors. Now turning to Sonia for the clinical update.

Thanks, Yannis. Turning to slide 14, we see the outline of the clinical design of the Phase 1 of IPH4502 study.

We are currently evaluating this asset in a first-in-human Phase 1 open-label, multicenter study in patients with advanced solid tumors known to express Nectin-4. We collect tumor biopsies at baseline from these patients and evaluate the Nectin-4 expression retrospectively.

The study started in January 2025 and runs at specialized cancer sites in the US and in France. This first-in-human study is guided by an adaptive BOIN design with backfill cohorts, with the objective to assess safety, tolerability, and preliminary antitumor activity.

Cohorts are backfilled at lower doses during the dose-finding trial, while prioritizing the dose-escalation cohort to explore a higher dose. These backfills help to generate more data in terms of safety, PK, efficacy at a given dose level.

Enrollment in the dose-escalation part of the study has progressed well, and Phase 1 dose escalation and cohort enrichment are nearing to completion, and the maximum tolerated dose has been reached. We have defined a clear therapeutic window with a favorable safety profile to date, and see preliminary efficacy at different dose levels within the defined therapeutic window in heavily pretreated patients with advanced solid tumors, including urothelial cancer patients who have progressed after enfortumab vedotin.

Turning to next slide, we see that we highlighted a growing therapeutic gap in bladder cancer after progression on EV plus pembro. Despite the advancement of enfortumab vedotin that has introduced in urothelial cancer patients, 2/3 of these patients still experience disease progression within two years, and the management of patients who progress to this regimen has become a critical challenge.

As of 2026, there is no single established gold standard for second-line therapy after EV-pembro, but several strategies are utilized based on patient-specific factors. For patients who received first-line EV plus pembro without prior platinum exposure, platinum-based chemotherapy—cisplatin or carboplatin with gemcitabine—is the preferred subsequent option.

Real-world data indicates modest efficacy, with a median real-world time to next therapy of approximately 3 to 4.7 months. Due to the limited efficacy of current second-line options, enrollment in clinical trials is strongly prioritized in 2026 guidelines to investigate novel mechanism of action and combination therapies.

This creates a significant unmet need in the post-EV plus pembro setting, and we believe IPH4502 is well positioned to potentially fill this therapeutic gap. In the next slide, we see our development vision for IPH4502, which includes both bladder cancer and broader solid tumor opportunities.

In bladder cancer, we see an opportunity to address the growing population of metastatic urothelial cancer patients who progress after EV-based therapies, where Nectin-4 expression appears to remain stable in tumor from patients who progress after EV. Over time, we also see potential to move to earlier lines, including in combination with anti-PD-1 therapy.

Beyond bladder cancer, we believe IPH4502 may also have potential across multiple solid tumors with low to medium Nectin-4 expression, and we intend to consolidate the signals observed in the dose-escalation study. 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.

Now, before we move ahead with our partner program, this slide highlights how we have built a comprehensive ADC discovery platform to develop a portfolio of next-generation ADCs designed to overcome the limitations of the current ones. Building on the IPH4502 linker, which stability in patients is clearly demonstrated by our emerging clinical data, we are developing a drug candidate portfolio around three approaches.

First, dual-targeted bispecific ADCs to address tumor antigen heterogeneity and to expand addressable indications compared to single tumor antigen targeting. Then, bispecific ADC with enhanced internalization to unlock the activity in the low-expressing tumors.

Finally, dual-payload ADCs using complementary mechanism of action to overcome resistance. Our next wave of ADCs is currently progressing towards candidate selection and then IND-enabling studies.

Now, turning to Sonia.

Turning to slide 19, we now provide an update on our AstraZeneca partner programs: monalizumab and IPH5201. In the next slide, let's start with monalizumab.

The PACIFIC-9 is a major Phase 3 randomized, double-blind study to demonstrate that dual immunotherapy can significantly increase the survival rate of patients with unresectable stage 3 non-small cell lung cancer who have not progressed following definitive concurrent chemoradiotherapy. The rationale for this trial is supported by three Phase 2 studies in early-stage non-small cell lung cancer, including COAST, NeoCOAST, and NeoCOAST-2 studies.

These studies reinforced the potential of targeting the NKG2A pathway to enhance the innate immune response alongside PD-L1 inhibition in early-stage lung cancer. Enrollment in PACIFIC-9 has been completed, and now we look forward to the data expected in the second half of 2026.

Now in the next slide, let's move to another asset, this time in the adenosine pathway, that is also co-developed with AstraZeneca: IPH5201, that blocks CD39, an enzyme that converts ATP into adenosine, which suppresses the immune system. By preventing this conversion, the therapy is re-energizing the immune system within the tumor microenvironment.

IPH5201 is currently evaluated in the MATISSE Phase 2 trial in combination with durvalumab and neoadjuvant platinum-based chemotherapy in patients with resectable non-small cell lung cancer. The recent pre-planned interim data presented at the AACR Annual Meeting on April 21st during a clinical trial plenary session has significantly strengthened the case for this anti-CD39 antibody.

The interim analysis of 40 patients demonstrated that the combination of IPH5201, durvalumab, and chemotherapy is achieving pathological complete response rates that compare very favorably to the current benchmark. The primary endpoint of pathological complete response showed a strong correlation with PD-L1 expression level, based on the robust 35.7% pCR rate in PD-L1 above 1%, and 50% pCR rate in patients with tumor with PD-L1 expression of at least 50%.

The study is now moving forward by focusing recruitment exclusively on patients with PD-L1-positive tumors. No new or unexpected safety signals were identified.

The combination was generally well tolerated, with most adverse events being grade 1 or 2. CD39-positive cell density in tumors is warranted to be further investigated as an emerging biomarker for predicting pathological complete response in IPH5201 plus durvalumab treatment.

Overall, these encouraging early findings support continued investigation of IPH5201 in non-small cell lung cancer.

Turning to slide 22, slide 22 summarizes the financial highlights of our AstraZeneca partnerships. For monalizumab, the agreements amount up to $1.275 billion of milestones.

We have already received $450 million and remain eligible to additional $825 million of potential payments. In case monalizumab is approved, AstraZeneca will book sales, and Innate Pharma will receive double-digit royalties on sales in the US and rest of the world.

In Europe, since Innate Pharma is contributing to 30% of the funding for the Phase 3 trial, we will get 50% of the profits and have the option to co-promote the drug. For IPH5201, the agreement 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, Innate Pharma has also the option to co-fund Phase 3 trial in order to get 50% of the European profits and co-promotion rights.

Otherwise, Innate Pharma will receive royalty in Europe like in the US and rest of the world. Together, these partner programs provide Innate with meaningful potential non-dilutive cash through future milestone, royalties, and profit-sharing economics.

I will now hand over to Jonathan for closing remarks.

Thank you, Yannis, Sonia, and Stéphanie. Turning to our upcoming milestones, over the coming quarters, we expect several important catalysts across our priority assets.

For lacutamab, we remain focused on initiating the TELLOMAK-3 confirmatory Phase 3 study in the second half of 2026, subject to financing. For IPH4502, the study is progressing very well, and we have observed preliminary antitumor activity with a favorable safety profile to date, including in patients with urothelial cancer relapsed or refractory to EV, which is a signal that we're starting to validate our preclinical hypothesis.

We look forward to continued maturation of the emerging clinical data set following completion of dose escalation and cohort enrichment. For monalizumab, the Phase 3 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. With a cash position of €25.4 million as of March 31st, 2026, we remain disciplined in our execution and focused on advancing programs that we believe have the potential to deliver meaningful value for both patients and shareholders.

With that, operator, we're now ready to open the call for questions.

Hi, guys. I have a question on MATISSE and CD39 since that was presented recently.

The discussant at AACR pointed out that while the triplet compares favorably to prior outcomes with durvalumab plus chemotherapy, looks pretty similar to prior outcomes with the PD-1s plus chemotherapy in the neoadjuvant setting. I wonder what gives you confidence given that sort of range of broader benchmarks, and in the next part of the MATISSE trial, is there a certain threshold of activity or biomarker finding that AZ and you are looking for to take it forward into Phase 3?

I think Yannis and Sonia between the two can answer. I don't know whether you want to start, Sonia, and then Yannis can fill in on the second piece.

Sure. Of course, you are right to say that this interim data show that the pCR rate that we observed at this interim analysis may be comparable to what has been seen in other trial using pembrolizumab.

When you are benchmarking, of course, with the same PD-L1 backbone that is durvalumab, you have to admit that there is a significant uplift over this therapy as a single agent. In that respect, this has definitely produced an increase of pathological complete response that is not matched by an increase of toxicities, which is remarkable.

We also seen that, for instance, in pCR high expression, this pCR rate goes even higher. Of course, we cannot predict where this trial may materialize in a Phase 3, but so far the data looks very promising.

Yeah.

Hi, Daina. Yannis is speaking.

Like Sonia says, this trial basically is providing two levels of information. First, that when you add CD39 on top of an active PD-1 blocker, it's increasing the pCR rate.

For us, it's clearly if the signal is confirmed on the additional patient, really validating the targeting of this checkpoint in the adenosine pathway, plus targeting I would say the efficacy of our drug candidate. Then whether AZ will decide to take their license on this one and move it into Phase 3, that's another question that is more actually for AZ.

From an Innate perspective, it's very important to confirm and to establish that the blocking of CD39 can be effective in that setting.

Great. Thank you.

Hey, thanks for the question. Maybe just two for me about 4502.

For the first question, are there any additional details you can give us on the profile of the drug at the go-forward dose? For the second question, what do you see as the most compelling indications outside of bladder cancer for the asset, considering market opportunity and potential competition?

Thanks for the question. At this moment, we can only say we have seen some efficacy readouts at different dose levels within the therapeutic window, and we will be a bit more specific around those dose levels, as well as potential indications to bring forward at a clinical conference this year.

Yep, got it. Thanks.

Thank you. This is RK from H.C.

Wainwright. Regarding the Nectin-4 ADC, it's just Lilly's product, which are in Phase 1, and Bicycle recently deprioritized their product.

How do you see the competition going forward? What sort of data would you be able to release in the next six months or so, we have an understanding of how you are poised against the competition?

Thanks for the question. In fairness, we don't know much about Lilly so far, and we can only speculate that perhaps the asset was deprioritized because it doesn't look as good as the other Nectin-4 program that they also have in clinical development.

We do not have the data because they have not been shared, and we can only see when the abstract will be available on the 21st of May. Sorry for not adding more color, but we don't have details.

Then in terms of the data, I think Sonia mentioned earlier we expect to present the data at a medical conference sometime later in the second half of the year. I think at that point, you will see go-forward indications and the data in urothelial cancer, and next steps for the program.

Thank you. Then on the collaboration with AstraZeneca, have you elected for the 30% funding on the PACIFIC-9?

Is there any residual cash obligations between you and them, between now and a positive readout?

Just to qualify a couple of things, the agreement that we have with AstraZeneca, it's capped at a certain level, and we are actually very close to the cap of the contribution, there are actually minimal contributions required between now and the data readout.

Okay. Thanks for taking my questions.

Great, thank you for taking our question. Two from our side.

Just any further color or perspective on the status of the lacutamab partnership discussions? Do you anticipate or feel confident that a deal can be finalized before the third quarter of this year?

The second question, are we expecting any Phase 2 PTCL data from lacutamab this year as well? Thank you.

Maybe on the partnerships, maybe I can start off, and Yannis can fill in any gaps. We are very confident that we will execute either a BD partnership or a royalty financing partnership for lacutamab.

The discussions are quite advanced, and we would expect to be able to conclude one of those two types of partnerships moving forward in the relatively short term. From our perspective, it doesn't really matter which way we go with either a BD partnership or a royalty financing partnership.

We would be running the Phase 3 confirmatory study, so that would be in our control, where we could utilize our expertise that we've developed in the CTCL area from the TELLOMAK-2 study. We'll make that decision in the coming future, basically based on what's best for the company in terms of the MPVs of the two different approaches.

Something coming in the future. Yannis, I don't know whether you want to

Short answer is yes, we are confident that we can execute something before Q3, yeah.

Just the second question around Phase 2,

yeah. The PTCL, as is run by the LYSA group, and we are towards the completion of this study, but I don't think that this data will materialize before the end of this year.

We have no further visibility on this study.

As this is an IST, it's under the control of the LYSA group, there's not a place where, as it's independent, we can have control of the timelines. We know that the LYSA group are quite excited about lacutamab in combination with the GEMOX chemo regimen, where they're studying this in late-stage patients.

We're optimistic that there will be data at some point in the future, but we can't put a very specific timeline on that.

Thank you.

Thank you, everybody, for attending the earnings call today. We're at a point in time where I think we have some very exciting catalysts coming over the coming months.

Just to remind you, on lacutamab, the initiation of the confirmatory Phase 3 program; for IPH4502, we're expecting to be releasing data on the first-in-human study at a medical conference before the end of the year; and then on monalizumab, we have the results from the primary endpoint of the PACIFIC-9 study coming before the end of the year. Thank you, everybody, for attending, and we look forward to giving you some updates in the very near future.

Thank you.