Good afternoon, everybody, and welcome to Jefferies 2025 Global Healthcare Conference. I'm Nausica Zunini from our healthcare investment banking team, and it's my pleasure now to introduce you to Jonathan Dickinson, CEO; Sonia Quaratino, CMO; Yannis Morel, COO; and Stéphanie Cornen, Investor Relations and Commercial Strategy Officer of Innate Pharma. Yeah, just a reminder, this will be a 25-minute presentation, and I'll hand it over to Jonathan. Thank you, and thank you to Jefferies for the invitation to present to you today. We're going to take you through a very quick overview of our portfolio and some of the key things that we're working on. Before we start that, this is the standard forward-looking disclosure statements which we'll be making today. Where I would like to start is a little bit of background on Innate Pharma. Innate Pharma has a deep experience in developing monoclonal antibodies. It was a spin-out from the Marseille Immunology Institute a number of years ago. Based on that expertise, the company has developed a series of clinical assets which focused on higher medical needs. If you look at those assets, we have a number today that are approaching what I would say inflection points, some of them close to the market and to the point where they can start to realize the commercial potential of those assets. A little bit of detail about the strategic focus of the company: we basically had a strategic refresh around about the middle of this year, which we announced with our half-year earnings. We actually have eight assets in the clinic, but what we've decided to do is to focus on three of those assets. Those assets are IPH4502, which is our highly differentiated Nectin-4 targeted ADC, which we're developing in solid tumors. It's lacutamab, which is our KIR3DL2 targeted antibody, which we're developing in cutaneous T-cell lymphoma. It's monalizumab, which is our NKG2A targeted antibody, which we're developing with AstraZeneca in stage III non-resectable, non-small cell lung cancer, and that's in a large randomized study today. At the same time that we focused in on those three assets and putting the majority of our time and attention behind those assets, we also have refocused our R&D organization, and we will be basically focusing moving forward on advancing our next ADCs. At the same time, we took a decision to make sure that our organization was fit for purpose, and we decided to downsize our organization by 30% so that basically our dollars, pounds, or euros, whichever currency you want to use, is going towards driving the programs rather than infrastructure. If we look in a little more detail at each of those assets, starting with lacutamab, as I said earlier, this is our anti-KIR3DL2 targeted antibody for cutaneous T-cell lymphoma. We have completed a phase II study, which is called the TELLOMAK study, and this study had a combination of mycosis fungoides patients and Sézary syndrome patients, which are two distinct subtypes of cutaneous T-cell lymphoma. The results from that study have led to a breakthrough therapy designation from FDA, and under that BTD designation, we've had a number of interactions with FDA. We've aligned on an accelerated path to approval for the Sézary syndrome indication, and more recently, we've aligned on the confirmatory phase III study that will be required to take advantage of that accelerated approval opportunity. Last week, we put out a press release announcing that FDA had given the green light for that study after we'd had their full feedback and endorsement. Basically what we have in our hands today with lacutamab is an opportunity where we have a de-risked path to approval. We have the data in our hands to be able to submit the BLA for Sézary syndrome. What we need to be able to do is set up a confirmatory phase III study to be able to show FDA that that study is ongoing and has a reasonable enrollment status, and then we can submit the BLA for Sézary syndrome. That's exciting for the company and potentially our first approval of a product coming out of Innate's research. The other exciting element of the confirmatory study is that it will not only confirm the indication in Sézary syndrome, but it will also provide the randomized phase III data required for a submission in mycosis fungoides, which is the bigger indication, and it will deliver that reasonably quickly. In the middle of the slide, we have monalizumab, and as I said earlier, this is the product that we're collaborating with AstraZeneca. This is being developed in non-small cell lung cancer in stage III non-resectable non-small cell lung cancer. The product is in a large randomized phase III study called the PACIFIC-9 study. That study is fully enrolled. It has completed a futility analysis at the end of last year and is heading towards the primary completion of the study in June 2026, with the data available from the primary endpoint early in the second half of 2026. This is another important inflection point for Innate Pharma. If that study is positive, it will basically result in $825 million of milestone payments, a mixture of regulatory, commercial, and development milestones due to Innate Pharma, a 50% profit share for Europe, and double-digit royalties on sales outside of Europe, including the U.S. We then have our Nectin-4 targeted ADC, IPH4502. This is a very highly differentiated Nectin-4 targeted ADC, and we'll give you some more details of that in a few minutes. It's basically differentiated at a number of levels, primarily with the antibody and the binding site, the epitope that we hit, which is different to any of the other Nectin-4 ADCs out there. What it basically means is that we can not only bind the high-expressing Nectin-4 tumors, but we can also bind the low and moderate Nectin-4 expressing tumors, which opens up a whole different range of tumor types where you can potentially develop this product, such as triple-negative breast cancer, prostate cancer, and basically some non-small cell lung cancers, some very significant tumor types where there will be very significant business potential. The other level of differentiation is based around the payload. We have an exatecan payload that comes with a different resistance and toxicity profile to most of the other Nectin-4 targeted ADCs, and that gives us an opportunity to develop this product in a PADCEV-resistant setting. I think you're all aware today PADCEV is selling $1.5 billion in the first-line setting. It's about to head into a line of therapy earlier in muscle-invasive bladder cancer, and that first-line setting will then be open to a product that will work in PADCEV-resistant settings. IPH4502 is potentially the perfect product to put into that particular setting. We're currently in a phase I study, and we're recruiting very quickly. We have hit a pharmacologically active dose, and we have started to see signs of clinical activity at that pharmacologically active dose. At that point, I'm going to hand over to Yannis, and Yannis will take us through a few more details of some of the preclinical evidence for IPH4502 and show you how it can be differentiated. Yannis. Good afternoon, everybody. Like Jonathan just told you, I'm going to show you why we think that Nectin-4 is really an ideal target for next-generation type of ADC, as well as the key differentiating properties of IPH4502, which is our proprietary ADC. As you know, Nectin-4 is a validated target for antibody-drug conjugate, where unfortunately PADCEV is approved in bladder cancer. The potential for this target is much broader than that because it's really expressed in a lot of various tumor types, but with a lower expression level than in bladder. Really, bladder is a bit of the outlier; it's where the high expressors are the most prevalent, but you have expression of Nectin-4 in esophageal, in breast cancer, in lung cancer, in prostate, so in many more tumor types than just bladder. So far, PADCEV has shown pretty limited efficacy beyond bladder. Also, in the bladder setting, it comes with some liabilities in terms of toxicity, like the peripheral neuropathy, and a lot of patients are undergoing either dose reduction or interruption of the treatment because they cannot really continue with the long-term PADCEV treatment. You may have seen also in the phase III, where PADCEV has been approved in combination with pembrolizumab, the overall survival is really impressive, but the PFS is still limited compared to the effect in the U.S., really showing that a lot of patients cannot continue over a long period of time the PADCEV treatment. What we have designed is a proprietary ADC with a new humanized antibody that is hitting a different epitope than the PADCEV and all the most known ADCs that are out there in clinical development. It has a high affinity and also very high internalization capability, meaning that it can bind, like Jonathan was saying, the medium and the low expressors. What we have done is that we have shifted the payload. PADCEV is using MMAE, so it's a tubulin inhibitor. We are using exatecan with a topoisomerase inhibitor, which has the great advantage of not being sensitive to the mechanism of resistance of MMAE. It has also a very good bystander effect so that it can kill the neighboring cells in case there is a heterogeneous expression of the Nectin-4 in the tumor. One of the difficulties of sticking eight exatecan and an antibody is that it's a molecule that is very hydrophobic, so you need to design a linker that can counterbalance the hydrophobicity of the payload. We have done that by generating a very stable and very hydrophilic linker that is able to mask the hydrophobicity of the exatecan. We have published at several big meetings like AACR, RCT, or ASCO various posters, but here, in a nutshell, they are the two main directions that we are pursuing in the clinical development. One, which is related to the post-PADCEV setting, which is on the left. You can see that, and it has been published also in the literature, that patients who are relapsing under PADCEV are not losing the expression of the antigen. The main mechanism of resistance to PADCEV is really related to the payload by the upregulation of a protein called MDR1. We have recapitulated that in a preclinical model where we have generated this model of secondary resistance, and you can see that on the left part, when we generate this model by chronic exposure to PADCEV, we generate a model that is no more sensitive to PADCEV, but where IPH4502 is inducing complete regressions of the tumor. We have tested, I would say, in a series of different PDX models, the efficacy of IPH4502 compared to PADCEV, and you can see that in some indications, like for example in head and neck, the efficacy is similar, but you have other indications where they are not responding to PADCEV and where IPH4502 is really inducing complete regression. Especially, as you can see in this model of esophageal cancer, where the expression is really low to moderate, there is absolutely no efficacy of PADCEV, whereas we have complete regressions with 4502. Now this asset is in phase I, and I will let Sonia describe to you where we are in this trial. Thank you, Yannis. Basically, we have built the first inhuman trial for IPH4502 based on the two main differentiating factors that we have seen in preclinical models. The first one is to enroll patients that may express low to moderate expression of Nectin-4 or have a heterogeneous expression of Nectin-4. You can see that the study population is basically a group of patients that may express a lower level of Nectin-4 compared to urothelial cancer patients. The second is to enrich this cohort of patients with urothelial cancer that may have progressed after PADCEV. This is an adaptive study design. It's a Bayesian design, and anytime we escalate, we have the possibility later on to enrich the cohorts of patients that we consider interesting to test the two main preclinical hypotheses. The study started at the end of January, and as we speak, we are already at therapeutic dose, and as Jonathan mentioned, we already see signs of clinical efficacy, and we are at pharmacologically active dose. The study then will progress by defining the optimal dose by selecting the two most promising indications and randomizing them to receive two different dose levels of IPH4502 to define the recommended phase II dose. Of course, the objective of the study is to assess safety and tolerability, but also understand the PK, the pharmacokinetics, as well as the clinical activity. Now, moving to lacutamab, this is anti-KIR3DL2 monoclonal antibody that Jonathan mentioned has recently gained a lot of momentum after having received breakthrough therapy designation and the clearance from the FDA to progress for phase III in cutaneous T-cell lymphoma. When we look at lacutamab and the way to develop this asset, it's not only going from or remaining in a niche indication, but it is really thinking big in the sense that, of course, the data that we have generated in the phase II, in the TELLOMAK data that were presented last year at ASCO with the long-term follow-up, paved the way for the phase III for the breakthrough therapy designation and the path for accelerated approval in a niche indication, which is Sézary syndrome. The phase III confirmatory trial, a randomized controlled study, will also provide the necessary data to reach an approval, a full approval in the much larger mycosis fungoides indication. Later on, we can really think of moving to life cycle management with PTCL, that is an aggressive lymphoma still with an unmet medical need, and we currently have a phase II ongoing of lacutamab in combination with chemotherapy conducted by the LYSA group. Now, when we look, let's have a look at the data that constitute the basis for the accelerated approval in Sézary syndrome. These are patients who all received mogamulizumab, that is the best drug that we have available for Sézary syndrome, and Sézary is the leukemic form of cutaneous T-cell lymphoma, a very aggressive disease with a very limited overall survival. There are no approved therapies with the exception of romidepsin and vorinostat, two HDAC inhibitors that have very little clinical activity that are approved in this setting. It is a very high unmet medical need. In this patient population, heavily pretreated post-mogamulizumab, our phase II has been able to demonstrate an objective response rate of 42.9% with a durability of response in excess of 25 months, so more than two years. For the whole patient population, a progression-free survival of 8.3 months. These are the data that were considered by the FDA a possible game changer for the treatment of cutaneous T-cell lymphoma in Sézary syndrome post-mogamulizumab. The phase II data also provided very interesting information on the larger opportunity, the mycosis fungoides. Here, it's getting interesting because in mycosis fungoides, usually only 50% of patients express a higher level of KIR3DL2, the target. The data that we have reported clearly demonstrate that there is no difference between patients that express more than 1% or less than 1% of the KIR3DL2, basically opening the path to enroll all comers into the phase III study. Indeed, we see that the global objective response, and the global objective response encompasses skin, visceral, blood responses, is around 19.6% for the two groups. A median duration of response of 13.8 months and a progression-free survival with no difference between the two groups of 10.2 months. That is, let's say, the longest seen in this patient population. Now, this is the study design that has just received green light from the FDA. This is an open-label, multi-center randomized comparative phase III study of lacutamab in relapsed refractory patients with cutaneous T-cell lymphoma. The study is in second line plus, and so it's one earlier line compared to the phase II, and it's enrolling two cohorts separately, the Sézary syndrome and the mycosis fungoides, with a separate analysis plan. Now, in Sézary syndrome, all patients have received pretreatment with mogamulizumab, and they are randomized to receive either lacutamab or romidepsin. That is the only approved drug in this, only FDA-approved drug in this setting. The primary endpoint is progression-free survival by blind independent central review, and the secondary key objective is overall survival. In the MF cohort, we also recruit patients who failed at least one prior systemic line, and patients will be randomized one-to-one to receive lacutamab or mogamulizumab. Again, the primary endpoint is progression-free survival, and key secondary endpoints are quality of life by the Skindex or pruritus because these patients experience a profound decrease of quality of life. The sample size has been estimated for these two groups to beat each relative comparator drug. Stéphanie will go through the commercial case. Thank you, Sonia. Now, if we move into the commercial opportunity, an important parameter to evaluate the commercial opportunity is, of course, the size of the eligible population. CTCL being a rare disease, the assessment of its prevalence and incidence remains a challenge, and that may underestimate the true burden of this disease. A few weeks ago, we held the Cowen event in New York where we invited ZS Associates, and they have presented the most up-to-date source of U.S. claims data for the CTCL population, and they highlighted that the incidence and prevalence in CTCL is much higher than what is reported in the public database. If we look at the Sézary syndrome, this is really the near-term de-risk opportunity in the U.S.. There are around 300 new patients each year, an overall diagnosed population of 1,000, and there are around 3,000 patients treated with mogamulizumab each year. This is really the population that we target through the accelerated approval. Interestingly, it will really be a clear and actionable commercial opportunity because this will be concentrated in specialized and referral centers that treat most of the Sézary syndrome patients, which makes it really a focused commercial footprint. If we move into MF, so the mycosis fungoides, here again, there is a higher incidence with what is reported in the public database with 3,000 new patients each year diagnosed, and a quarter of them are treated with systemic therapy. The objective of the phase III is really to establish lacutamab as a standard of care in the second-line setting in this population, and this is supported by the primary physician research that we have run. Importantly, the launch infrastructure that will be for SS will enable an efficient expansion into MF because this is a shared prescriber network between MF and SS. Here, we look at the market potential for lacutamab. For the Sézary syndrome, we see an opportunity up to $150 million in the U.S., which is the indication targeted for the accelerated approval. The second indication, mycosis fungoides, will lead us to up to $500 million in the U.S. and Europe. The third bucket, I will say last but not least, represents an even broader opportunity because as a life cycle management plan, we really see an opportunity for lacutamab to treat the early-stage patient. For this patient, if you have a drug that is improving their quality of life because it removes their symptoms like the itching, the fatigue, the skin lesion, it controls durably the disease and is very well tolerated, you can offer a systemic drug that will be available for this early-stage patient early on in their disease journey. This will open the market for CTCL. Now I am handing over to Jonathan for the conclusion. Thank you. I'm going quickly because I think we're more or less out of time. Just a few words about monalizumab. This is the design of the study, the PACIFIC-9 study, which is being conducted by AstraZeneca today, which basically is due to read out in primary completion June next year and then primary endpoint results early in the second half of next year. Just to give you some information on what that was based, it was based on this study, which is the COAST study. This was a randomized phase II study. Basically, when you added monalizumab to durva, it added about 12 months median PFS in addition to that of durva. If you carry a reasonable proportion of this effect size into the PACIFIC-9 study, we should, in theory, have a positive study. This was a very significant effect size seen in the phase II study. Just to remind you of what is due under the terms of the deal, $825 million in milestones, a mixture of development regulatory of $400 million and then commercial of $425 million, 50% profit share for Europe and double-digit royalties on sales outside of Europe, including the U.S. market. In terms of key takeaways, we have a number of catalysts coming for Innate Pharma. The key one is really around IPH4502. We are at a pharmacologically active dose now. We are in the phase I dose escalation stage, and we should have data sometime early H1 next year. That is a pivotal point for lacutamab. We have the initiation of the phase III study, which should come during the first half of next year and counts down the start of the clock to submission of the BLA for the Sézary syndrome indication. As I mentioned just before, we have the PACIFIC-9 results due at primary endpoint just after the second half of next year. In terms of catalysts, some really important ones from an Innate Pharma perspective coming very quickly. With that, we'll close the presentation and thank you for your time and your attention.