I would like to hand the conference over to your speaker, Mondher Mahjoubi. Please go ahead. Thank you. Good morning, good afternoon, and welcome everyone. Really pleasure to be here with you today. This morning, we issued a press release providing a business update for the first half of 2021. I look forward to explaining the progress we have made during the year to date, as well as addressing future goals and milestones. The press release and today's presentation are both available on the IR section of our website. Before we start, on slide two, I would like to remind you that we make forward-looking statements regarding the financial outlook, in addition to regulatory and product plan development. These statements are subject to risks and uncertainties that may cause actual results to differ from those forecasted. On today's call, I'm delighted to be joined by Dr. Joyson Karakunnel, EVP and Chief Medical Officer, and our CFO, Frédéric Lombard, who will present an update followed by a Q&A session. On slide four, you have the classic intro slide of Innate Pharma. As you know, we are pioneers in the field of innate immunity, and in particular in NK cells. We follow the science to develop innovative therapeutics for patients, leveraging our know-how and antibody generation platform. We are using this expertise to develop a robust pipeline of novel medicines for cancer. Please move to slide five. Our pipeline shows how we have translated this scientific leadership into a robust portfolio of both proprietary and partnered assets. It also illustrates how we are executing against our strategy with our lead asset, lacutamab, supported by partnered and also earlier stage products. Additionally, we have a rich pipeline, including the adenosine pathway with an anti-CD73 and an anti-CD39 in the clinic. A pool of preclinical projects, including our ANKET natural killer engager platform, which we will carefully select and bring forward and fuel our clinical pipeline. Please move to slide six. Our strategy centers around three core priorities, where we look to drive value from our early R&D efforts through later stage partnerships where it makes sense to do so. First, we look to create near-term value driven by our lead proprietary product candidate, lacutamab, which is in development for T-cell lymphoma. Second, fueling our pipeline and creating longer-term value by leveraging our antibody engineering capabilities to develop innovative molecules with a primary focus on our multi-specific natural killer engager platform delivered from our proprietary ANKET platform. Third, we are building a strong and sustainable foundation for our business, leveraging various partnerships across industry and academia. We will look to partner, including in late stage, when it makes sense to do so. This will further validate our science and offer capital that we can reinvest to advance our early portfolio. During the first half of this year, we have worked diligently to execute against these three core priorities. Number one, we have continued to advance lacutamab as we pursue a broad development strategy across T-cell lymphoma. We were excited to showcase lacutamab data in mycosis fungoides from the phase II TELLOMAK trial at Lugano, and we have progressed to stage two earlier than anticipated. In addition, we announced our stepwise approach in developing lacutamab in PTCL, with two clinical studies for KIR3DL2 expression patients with relapsed peripheral T-cell lymphoma, including a randomized controlled trial in collaboration with our partner and the leader of Lymphoma Study Association. We have also worked hard to advance our R&D efforts with our early stage program moving forward. We were pleased to announce earlier this year that Sanofi made the decision to progress IPH6101, our lead natural killer engager into R&D enabling studies. This is the first candidate to emerge from our multi-specific NKCE natural killer engager platform, and we are very excited by the prospect of this technology, which we believe will fuel our pipeline well into the future. We look forward to telling you more about our progress here later in this call and in the near future. Lastly, we look for further updates on our monalizumab collaboration with data from the randomized phase II COAST trial in stage three unresectable non-small cell cancer, which will be presented at ESMO this week. I would like now to pass the call over to Joyson, who will review the progress made with our portfolio, starting with lacutamab, our lead proprietary asset. Joyson? Thank you, Mondher. On slide seven, let me start with lacutamab, our first-in-class humanized monoclonal antibody that targets the immune receptor KIR3DL2. As you may remember, KIR3DL2 is an inhibitory receptor found in approximately 65% of patients across all cutaneous T-cell lymphomas and even more in certain aggressive subtypes, but with limited expression in healthy tissue. To date, data from lacutamab have shown promise, demonstrating compelling single-agent activity and offering immense potential in lymphomas historically associated with a poor prognosis for which there are a few therapeutic options at an advanced stage. On slide eight, I just wanted to remind you of our development strategy for lacutamab in T-cell lymphoma. We are pursuing a fast-to-market strategy with a potentially pivotal trial underway in a niche setting of Sézary syndrome, where lacutamab was granted U.S. Fast Track designation, EU PRIME designation last year. We are also looking to potentially expand past Sézary syndrome to mycosis fungoides, where we have encouraging preliminary data from our phase II trial, which I'll cover in a minute. Finally, we are advancing into peripheral T-cell lymphomas with a couple of recently announced trials. On slide nine, let me highlight the great progress we have made this year in our ongoing phase II TELLOMAK study for Sézary syndrome and mycosis fungoides. In mycosis fungoides, firstly, we moved the KIR3DL2 expressing cohort from stage one to stage two, clearing a predetermined threshold before 50% of the cohort was enrolled. The KIR3DL2 MF data was also presented at Lugano, with the next MF data due in 2022. For the Sézary syndrome cohort, enrollment is on track, and we expect to be able to report top-line data in 2022. On slide 10, we have a summary of the cohort two mycosis fungoides data in KIR3DL2 expressers. Here we see the preliminary results of cohort two, which showed an overall response rate of 35% in these late-line patients with limited treatment options. You see the median follow-up is still short, 4.8 months. It is important to consider that there are quite a lot of confirmed responses. We now have six confirmed responses out of 17. You see that some patients have quite a long duration of follow-up in this cohort two. If we look at the response by compartment in the skin, you see that the responses are quite high, now with 11 confirmed responses out of 17. These skin results are extremely interesting because skin is very important for quality of life of the patient. It is interesting to see that the majority of patients had represented a very good complete or partial response in the skin. We are encouraged by the data and look forward to further proof points in 2022. On slide 11, as mentioned, we are working to advance our recently announced clinical development plan for peripheral T-cell lymphoma, which will focus initially on the relapse setting where the unmet medical need is most significant. We are initiating our phase Ib trial evaluating lacutamab as a monotherapy by mid-year. The study will enroll approximately 20 patients and will evaluate safety and characterize clinical outcome. First data are expected in 2022. Separately, our partner, LYSA, are initiating an investigator-sponsored phase II study to evaluate lacutamab in combination with the chemotherapy GemOx. This study will be a multicenter randomized trial with approximately 60 relapsed refractory patients outside the U.S. We believe that this stepwise approach will prove efficient in identifying the optimal regimen for lacutamab in the relapsed PTCL setting. Depending upon the data generated in these initial studies, we will consider initiating a separate trial in combination with another standard of care treatment, and eventually, we would look to move lacutamab into earlier lines of treatment, including as potential combination in the CHOP regimen in the frontline PTCL or as a consolidation therapy following standard first-line treatment. Moving on to slide number 12. We are pleased to have presented our latest innovation to our proprietary multi-specific NK cell engager platform that we call ANKET, which Eric Vivier presented at the FOCIS meeting in June, and for which an oral presentation has been accepted for ESMO this week. ANKET stands for Antibody-based NK Cell Engager Therapeutics. These multi-specific molecules are made of various building blocks, as is illustrated here. The reason why we are so excited about the ANKET is because we are announcing two breakthroughs. First, a technological breakthrough, and second, an efficacy breakthrough. This is leading to the harnessing of NK cell effector function against cancer and also provides proliferation. On the technological breakthrough, as you can see on this slide, ANKET is very versatile, fit for purpose technology that is creating an entirely new class of tri and tetra specific molecules to induce strategic immunity against cancer. On the efficacy breakthrough, this unique NK cell engager engages for the first time two activating NK cell receptors, namely NKp46 and CD16, but also the combination of receptors for IL-2, IL-2R-beta, and IL-2R gamma. With the IL-2 variant and tumor antigen in a single tetra-specific molecule. Overall, it demonstrates a better anti-tumor efficacy than clinically approved antibodies within the limit of preclinical models. On slide 13 is a summary of the data on our recent generation of tetra-specific ANKET, which is made of four components. In yellow, an antibody fragment that recognizes the tumor antigen. In green, an antibody fragment that recognizes NKp46. In red, an Fc portion that will interact with CD16. In blue, a variant of the interleukin-2 IL-2 variant. On the left side of the graph, we show you the contribution of the tetra-specific ANKET with the IL-2 variant. The black graph on the far left is the vector. The green graph is the tetra-specific ANKET, and the red graph on the right is a tri-specific ANKET with the IL-2 variant separated. You can see the benefit from the green graph in the middle of including the tetra-specific ANKET with the IL-2 variant. On the right, you can see the benefit of tetra-specific versus the vehicle obinutuzumab in lung mouse models. On the top, you have the vehicle, in the middle, tetra-specific ANKET, and on the bottom, the CD20 obinutuzumab. Activity is seen with the tetra-specific model that is not seen with obinutuzumab. We look forward to updates on ANKET this year at ESMO and other scientific congresses and look forward to progressing our partnership with Sanofi. Finally, on slide 14, we have our third pillar of our strategy of building sustainable business. I wanted to highlight the latest developments for monalizumab, which we have out-licensed to AstraZeneca and received EUR 400 million in milestones to date, with further potential milestones due. To remind you, monalizumab is an anti-NKG2A, which acts upon the checkpoint pathway to potentiate NK cell activation. This is being trialed in combination with cetuximab in head and neck cancer, and also in combination with the anti-PD-L1 immunotherapy durvalumab in lung cancer. In head and neck cancer, the phase III INTERLINK-1 trial of monalizumab plus cetuximab in IO pretreated head and neck cancer is underway. In addition, we are expecting data from cohort three of the phase II trial later this year for the triplet of monalizumab plus durvalumab plus cetuximab in first-line head and neck cancer. As mentioned previously, the phase II data in stage three non-small cell lung cancer COAST trial for monalizumab in combination with durvalumab will be presented at ESMO this week by AstraZeneca. In summary, we look to work further with our partners at AstraZeneca. I will now hand over to Frédéric to cover the financials for the half. Thank you, Joyson, good day, everyone. Moving to the finance slide 15, I will start with one of our key metrics as usual, our cash position. Our cash and cash equivalent amounted to EUR 159.4 million as of June 30 this year, down from EUR 181.7 million at the end of Q1 2021. We are in a strong financial position with cash to fund planned operation to at least 2022. In addition, as you can see, we are efficiently managing our resources and sizing opportunity to accelerate our impact by nimbly following data to explore strategic and opportunistic indications. We believe this approach ensures that we remain in position to strategically invest in our vision for Innate. Now, going into the P&L, I will only comment on the main and most significant lines, and you have very detailed comments in the appendix of the press release that you can refer to for more information. I start with our revenue for collaboration. Our revenue and other income amounted to EUR 15.7 million, and the main resulted from revenues from collaboration and licensing agreements, and to a lesser extent, from governmental funding. This revenue mainly results from the spreading of the upfront and opt-in payments received from AstraZeneca for monalizumab, which I remind are recognized on the basis of the percentage of completion of the work performed by the company. I also remind you that it has no impact on cash. On operating expenses. For the first half of 2021, they amounted to EUR 41.1 million, a reduction of 11% from the first half of 2020. R&D expenses decreased by EUR 9.7 million to EUR 21.8 million, representing just over half of our operating expenses. This change mainly results from a decrease in depreciation and amortization expenses allocated to R&D following the end of the transition period with AstraZeneca in September 2020. The return of commercialization rights in the US and Europe for Lumoxiti, as well as the end of the recruitment in trials evaluating avdoralimab in oncology. Turning to SG&A expenses, they increased by EUR 4.8 million to EUR 19.3 million for the period, primarily as a result of the provision for charges booked relating to the payment of $6.2 million to be made to AstraZeneca in April 2022 under the Lumoxiti transition and termination agreement. This is less than the company reported up to $12.8 million contingent liability at the end of 2020, which was linked to the split of certain manufacturing costs. As such, net income from distribution agreements was nil following the end of the transition period relating to the commercialization of Lumoxiti in the U.S. The company recognized $1 million net sales of Lumoxiti for the first half of 2021. With that, I will turn back to Mondher. Thank you, Frédéric. Thanks, Joyson. Please move to slide 16. As you can see, we are working diligently to execute across all our strategic pillars and believe that we are laying the foundation to drive near and long-term value for our patients and our shareholders. Looking at our clinical program, we expect to achieve a number of milestones over the next 18 months. As you've heard from Joyson, our phase II TELLOMAK study for lacutamab continues to progress, and we expect to report potentially pivotal data in Sézary syndrome and in mycosis fungoides in 2022. In addition, we are moving our PTCL program into the clinic, with initial data expected as well in the next year. For monalizumab, we look forward to the phase II COAST data at ESMO this Friday, which builds on the hypothesis of adding monalizumab to the anti-PD-L1 durvalumab. Later this year, as you've heard from Joyson, we will present the data from cohort three of the phase II in head and neck cancer study, testing the combination of monalizumab with cetuximab and durvalumab in IO-naive patients with advanced head and neck cancer. We are further advancing the adenosine pathway agent in the clinic, where we are starting a new phase I trial for IPH5301, the anti-CD73, and we look forward to data from the anti-CD39 IPH5301 due in 2022. In parallel, we continue to develop our ANKET technology platform, we are very encouraged by the preclinical results from our next generation NK engager. We believe that this represents a natural evolution of our platform, illustrating the potential for all of NK cells, and the fact that they could become the next generation off-the-shelf cancer immunotherapy. With more to come, as Joyson said, this Saturday is another presentation at ESMO by Eric Vivier. We look forward to further updates on the progress of our ANKET platform in the second half of this year. Please move to the conclusion slide number 17. As you can tell, we have an exciting journey ahead at Innate. We continue to build our business to create value for patients and stakeholders. In summary, we have positioned Innate Pharma for the future with this refresh strategy and made meaningful progress throughout the year. Just to recap in summary, lacutamab, we moved forward with our MF trial and presented encouraging data at Lugano. Next year, we will have data on MF and potentially pivotal data in Sézary syndrome. We will start the PTCL trials. Second, our R&D engine was further validated as Sanofi chose to progress SAR443579 into R&D enabling studies. We will continue to leverage this antibody capability to develop innovative molecules with a primary focus on our next generation ANKET, NK engaging molecules, as also demonstrated at FOCIS and ESMO this year. Finally, as you heard from Joyson, we continue to build the sustainable business by balancing our portfolio with partnered assets that provide substantial revenue stream to support our continued investment in early R&D. Collectively, we are driving value across our business and ultimately advancing our goals to deliver innovative medicines to patients. We look forward to keeping you updated on our progress. With that, I conclude the prepared remarks, and I will now open the call to questions. Operator? Thank you. If you wish to ask a question please press star one and wait for your name to be announced. If you wish to cancel your request please press the hash key. Once again, star one if you wish to ask a question. We're taking our first question from the line of Daina Graybosch. Please go ahead. Hi. Thank you for the question. Two from me. One, just thinking ahead for the monalizumab data to be presented on Saturday. I wonder if you could remind us how much overlap in efficacy and read-through from proof of concept to proof of concept study do you believe there is when you combine monalizumab with durvalumab versus cetuximab? Does either of these therapeutic combinations or mechanisms bias the activity, the CD8 cells or NK cells. In addition, keeping alive my treatment, could we see NeoCOAST data this half? I notice it's not on your milestone slides, maybe you don't have specific visibility. Just wondering if it's a possibility it will come. Thank you, Daina. I'm going to repeat the question because the line was not great, so to make sure that I got it right and everyone also can hear them. You asked question on the NeoCOAST data, when this data will be public. Your first question was about the potential read across or read through from the COAST data to the INTERLINK trial and the combination of monalizumab with cetuximab. Correct. Am I repeating correctly? Okay, perfect. I'll start with the second question very quickly, to say that as you know, the NeoCOAST data is run by AstraZeneca. It's sponsored and run by AstraZeneca. We have really no further information than what is publicly available on the AZ site, which is that the data are expected in the second half of 2021. We will hear more probably from AZ in the near future. With regard to your first question, I think this is an excellent opportunity also for us to remind you our strategy from the basic research and the slide that Joyson showed to illustrate his remarks on monalizumab. You have two mechanism of action that were developed in our labs. The first one is a way to enhance the ADCC of antibodies that like cetuximab could have a synergistic effect when combined with monalizumab. That's what led to the head and neck program and the phase III trial that was started last year. The second piece of information and piece of data that was published already in Cell in 2019 was basically the preclinical package that supported the clinical program of the combination of monalizumab and anti-PD-1 or PD-L1, showing the clear synergy coming from the fact that, as you know, NKG2A is not only expressed on NK cells but also on a subset of CD8 positive T- cells. First of all, I think the two trials and the two setting and the two type of combination are supported by a strong scientific rationale. As you know better than me, these are two different tumor types and two different settings, and it's really premature to first of all speculate on the data before the COAST data are presented. Of course, I would be very cautious not to have a cross trial comparison or read across. I'll hand over to Joyson who can maybe complete this answer. No. I think Mondher summed it up very nicely. I think the strength of the preclinical data that supported these trials both with cetuximab as well as with durvalumab have two different mechanisms of actions that we look for the combination potentials. We've already kind of seen some of that with head and neck, and we'll have to wait for the data to see what happens with COAST. I think second, I think Mondher pointed it out very nicely, which is these are two different indications, two very different settings. One adjuvant, the other metastatic. It would be hard to read across the trials or read across trial comparisons, not only because we try not to do that, but also just because of the differences in indications, settings, as well as mechanisms of action. Thank you, Joyson. Does it answer your question, Daina? Yes, it does. Thank you very much. Thank you. We're taking our next question from the line of Yigal Nochomovitz, Citigroup. Thanks, Mondher and team. I just had a few questions. First, I know obviously you can't disclose the data yet on the ORR and PFS for COAST ahead of the late breaking presentation. That said, to the extent that you can comment generally, what% improvement in ORR and PFS would you view as clinically meaningful benefit for monalizumab plus durvalumab combo over durvalumab monotherapy? Thanks. Thank you, Yigal. Again, we look forward to seeing the full data presented at ESMO as an oral late breaking abstract. This was detailed by AstraZeneca and their curtain raiser. They will report ORR, but they also present PFS data for both arms, durvalumab plus monalizumab and durvalumab plus oleclumab versus standard of care. I think the design of the trial is well known. It has been already publicly disclosed. It's a well-controlled randomized phase II trial. They have not to my knowledge publicly disclosed the details of the statistical hypothesis. But I believe what is interesting to have in mind is that these are patients who finish their chemo radiation therapy and are randomized within six weeks if they do not progress. They are being treated with durvalumab for up to 12 months. The response rate is certainly a very important endpoint and is the primary endpoint for this trial. The quality of the response, and in particular, the disease-free survival or the progression-free survival, is certainly something to look at as well. I believe the response rate is certainly important to assess and we look forward to seeing those data. I think the PFS is something also to keep in mind. Okay, got it. Thank you. A second question I had on lacutamab. Can you talk a bit about how you're planning to identify Sézary syndrome and mycosis fungoides patients, given that in the major pharma markets, U.S., Europe Five, and Japan, there are only 200 Sézary patients and about 3,000 mycosis fungoides patients, according to the SEER database? Just to make sure I get your question. Is it vis-à-vis the commercial opportunity or talking in general about how we are designing and implementing or executing our clinical trial? No, more about the commercial opportunity. Yeah. Okay. Yeah. Thank you. This is of course, a great question and gives me the opportunity to go back to our strategy. I think the Sézary syndrome indication came as a prototype indication, if I can say, to validate the mechanism of action, since the majority of these patients are expressing KIR3DL2. We have seen in the phase I, basically from the first dose level, that when you target this tumor antigen KIR3DL2 you get significant tumor shrinkage and even an improvement in quality of life. I think the Sézary syndrome itself is the, how to say, the first step, and I should say the fast-to-market strategy in order to really get those Fast Track designation and PRIME designation and exchange with the FDA and with EMA in order to accelerate the clinical development. The intent, of course, is to expand beyond that. The mycosis fungoides is half of the PTCL. As you know, you are right. Mycosis fungoides accounts for about 3.5 to max 4,000 new patients every year in the U.S. and in Europe and Japan. There are about 4,000 non-mycosis fungoides cutaneous T-cell lymphomas. All in all, we're talking about up to 8,000 patients with cutaneous T-cell lymphoma. Half of them would express the KIR3DL2. Again, the mycosis fungoides segment is not the end of the story. It's certainly much more attractive and much more compelling business case. Of course, I think the most important milestone of the Lugano meeting was that we have been able to show that lacutamab works outside Sézary syndrome and it works in T-cell lymphoma, which express the KIR3DL2, which of course solidifies, if I may say, the scientific rationale to expand now to peripheral T-cell lymphoma where the business case stands, of course. With more than 18,000 new cases every year, peripheral T-cell lymphoma has a much more attractive commercial prospect. Again, the stepwise approach is to validate the mechanism of action, check that this is not a Sézary syndrome drug, but it works outside Sézary syndrome, which we are exploring and validating as we speak in TELLOMAK, and then go to peripheral T-cell lymphoma. When you look at the totality of the business case, it's no longer a niche indication. It's a significant market opportunity. Got it. Thanks. I have one final question. This one might be good for Frédéric or Joyson. I'm just curious about the ANKET platform and the choice of combining NKp46, CD16, and IL-2R. Is the thought that this tetra-specific asset would be better suited to solid tumors or to hematologic malignancies, or are both categories under consideration? Yeah. That is another excellent question that of course we debate internally, and I will hand over to Joyson to sum up the thought behind the selection of the tumor antigen for this multi-specific antibody. Joyson? Yeah. Thanks, Yigal, for the question. Yeah, I'm going to kind of go back and talk a little bit about the ANKET platform. The amazing thing about the ANKET platform is it's very versatile. As you were stating, the NKp46 CD16 attachments to the NK cells with the IL-2 variant in the same. The tumor antigen is what I call as removable. You could kind of put different tumor antigens in there. This allows for that flexibility. As Monder said, there's heavy debates going on internally to determine sort of what is the best approach. We are looking at both solid tumors as well as hematologic tumors. The versatility of the platform allows for us to kind of really have those debates internally to see which would be the best opportunity either in solids or hematologic malignancies. Thank you very much. Did that. Okay. Thank you. If you wish to ask a question please press star one and wait for your name to be announced. If you wish to cancel your request please press the hash key. Once again star one if you wish to ask a question. We're taking our next question from the line of Graig Suvannavejh at Goldman Sachs. Please go ahead. Hey, good afternoon. Good morning. Thanks for taking my questions. I've got a couple. First is actually on IPH5301. Certainly will be interested to see what the oleclumab data is for the AstraZeneca compound. Could you remind us how to think about differences that you are aware of between their asset and your asset? That's my first question around IPH5301. The second of all, as it relates to the COAST data, anything at least from a scientific or biological rationale that would help us think about how to think about monalizumab and the efficacy and safety that we might see relative to a CD73 targeted asset such as oleclumab. That's the second question. Maybe just a question on the P&L. How should we think about trending over the next several quarters, just given the many moving parts and in that context, as we think about your current cash balance where you say you have cash at least until 2022? I mean, we're right around the corner. How is the company thinking about financing options? What kind of options are available and what's the strategy? Thanks. Thank you, Graig. Very important and good questions as usual. I'll start with the first one then hand over to Joyson for the COAST and the mechanistic approach you're thinking about in particular with regard to the potential combination with anti-CD73. I'll give the opportunity to our new CFO, Frédéric, to address your question about the financing moving forward. Very briefly on IPH5301. As you said, we do really look forward to seeing the oleclumab data. I remind you, other than those data actually we are not aware of other public randomized data in this field. Everyone remember the Bristol Myers Squibb and the AG phase Ib data presented about two years ago at ASCO and AACR showing some trend of activity but nothing since then. Clearly the results of the COAST trial with regard to the oleclumab arm are of major interest for us and for the other companies that are playing in this field. Number two, I remind you that we published that data and again, we have even presented those data at AACR back in 2019, if my memory is correct comparing our anti-CD73 with the BMS and the AZ ones. Clearly when it comes to the enzymatic activity, our antibody is much better. It's superior in doing the job of blocking the anti-CD73. Of course, we have to translate those preclinical strength into clinical benefit for patient and that's why we were to some extent waiting to see some data emerge in order to try to learn from others. We have been working over the last couple of months in transforming the IND that we filed at the end of last year into a clinical trial, which is about to start soon. That would be our first clinical trial testing and assessing IPH5301. We have a plan on what combination approach we should do and of course we look forward to seeing the data from the COAST trial to further fine tune and also maximize the opportunity around our anti-CD73. That's my answer for the first question. Joyson, the question around COAST. How do we think to the extent of course I don't want to speculate on the data, but the mechanism of action and the potential combinability with an anti-CD73 if the two arms are effective. Yeah. I think I'll go back and kind of also state that the mechanisms of action here clearly as we know, are different. One's an anti-73, one's an anti-NKG2A. We have preclinical data that has supported ADCC synergy and then finally with monalizumab it's sort of non-redundant pathway mechanism of action and combination. I think when we look at this, we see, once again, two different tumor types. Same setting, two different mechanism of actions that do have different potentials. I think when it comes to the clinical data, I think we'll have to wait to see what the COAST data shows. I would just say these are two very distinct mechanism of actions operating in two different ways. Sorry, both of them relieving immune suppression. Sorry, I just messed up the cetuximab question, but this was CD73. With CD73, it's basically relieving of the tumor, the amount of adenosine that's present, so really decreasing immune suppression. Decreasing adenosine is one. The other one is decreasing in two different pathways, one anti NKG2A and the other one with PD-1. I think with that, we'd have to wait for the clinical data to see what's happening. I know that was a little roundabout messed up answer, so I'm happy to repeat it because I think in my head I had cetuximab and I was like, "Oh, gosh, this isn't cetuximab." Clearly I'm excited about both of these and I'm sitting here going, okay. Yeah. In short, the CD73 is adenosine. You're really stopping adenosine synthesis and so because of that, relieving the immune suppression. The other is two pathways, one acting on T-cells, the other one on NK cells. I think the clinical data will speak for at least which pathway may be better. I think that last answer is the one I would kind of go with versus my first. Okay. Thank you, Joyson. Thank you. Frédéric, would you want to take the question on what's the plan and the financing of the company moving forward? Yeah. Thank you, Mondher. Yeah, as I said before, the cash position is quite robust at the moment with EUR 159 million. We constantly monitor our financial needs. We provide an update when needed. We cannot communicate at this stage. In terms of plan, for sure, if you look at the cash burning for this first half versus last year, we see a big decrease. It's not following this investment. On our side, we keep our plan as planned, let's say. Last year was having some special cash burn related to Lumoxiti and special payments that we had at the same time. Today you will see a slight increase in the second half due to the delivery of some studies that we are having in the pipeline. Just in terms of how you're thinking about potential options to extend the cash runway. At the moment, first of all, we Mondher? You want me to? Yeah, please. Go ahead. Yeah, okay. The different options are, we look at the market for sure. We look at financing options also with some banks as well. More than ever, we look at progressing the way we operate and see what we can get out of those partnerships. Yeah. Graig, long story short, we have a solid cash position, we have a pretty good track record on making sure that our cash cover the multiple catalysts and milestone that we have ahead of us because we constantly monitor our financing needs, and we will provide an update when needed. Thank you. Thank you. Operator, do we have more question on the line? Yes, we have one question from Arthur He from HCW. Please go ahead. Your line is open. Hey, good morning. Hey, good afternoon, Mondher, and greeting to the gentlemen. Thanks for taking my question. I just wonder one question on the monalizumab, for the data going to be reported for the IO naive patients later this year. Could you remind us what kind of data set we could expect and how many patients we could look into the data? Thank you. Yeah. Joyson, would you like to answer or I can take it? Okay. No. Yeah, go ahead, Mondher. Go ahead. Yeah. Okay. Thanks, Joyson, for the question. First of all, to remind everyone, this is a single arm study that tests the triplet combination. Again, as I said in my answer to the first question, we have those two mechanism of action. We know that monalizumab could be synergistic with antibody that have or act within ADCC, and that's the combination with cetuximab. We know that monalizumab is synergistic with an anti PD-L1, and the COAST data were based on that rationale. I think the triplet is simply the combination of both cetuximab and durvalumab to see whether we can have an increase in response and in quality of response in terms of durability. The study was designed really, first of all, to assess the safety of the triplet because this, I remind you, this is the first, I believe, ever triplet IO to be developed or triplet of non-cytotoxic or chemo-free regimen to be developed in head and neck cancer. The safety was good for the first 20 patients, so we expanded the trial to 40 patients, but yet it's still a single-arm trial in advanced relapsed or metastatic patients with squamous cell carcinoma of the head and neck, who might have been pre-treated with chemotherapy or radiation therapy, but who are naive of any PD-X treatment. The data will be presented at the end of the year, and we are looking at the totality of the data with AZ to really determine what's the path forward. As you know, the competitive landscape is evolving, and it's important to take into consideration actually the specific unmet need and where we can position this triplet. Again, I insist on the fact that today the standard of care is pembro, plus or minus chemo, dependent on the level of CPS and the results that we are presenting at the end of the year will be looked at also from that perspective, CPS more than one versus CPS low or PD-L1 negative. We will be delighted to share this data, as I said, toward the end of the year. Thank you for that, and congratulations on the progress. Thank you very much. Thank you. Operator? Thank you. Any Thank you. Any further question? There are no further question on the phone. Okay. Henry, do we have question on the webcast? No more questions, Mondher. Thank you. Great. If there are no more questions, I would like, again, to thank everyone for dialing in this morning, this afternoon. I'm very excited with, again, the progress we are making with our strategy. As I said, we have encouraging data with lacutamab. Our R&D is progressing nicely with the new data from our ANKET platform, and we also all look forward to the continued progress, including the upcoming monalizumab presentation at ESMO this Friday. With that said, I look forward to talking to you in the near future. Thank you very much, and have a great day. That conclude the conference for today. Thank you for participating. 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