Good day, and thank you for standing by, and welcome to the Innate Pharma Half Year Results Conference Call. [Operator Instructions] For your information, the conference is being recorded. Now, 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 of the first half of 2021. I look forward to explaining the progress we’ve made during the year-to-date as well as addressing future goals and milestone. The press release and today's presentation are both available on the IR section of our website. And before we start, on Slide 2, I would like to remind you that we will 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, Frederic Lombard, who will present an update followed by the Q&A section. On Slide 4, 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 patient, leveraging our know-how and antibody generation platform. We are using this expertise to develop a robust pipeline of novel medicines for cancers. Please move to Slide 5. Our pipeline shows how we have translated the scientific leadership into a robust portfolio of both proprietary and partnered assets. It also illustrate how we are executing against our strategy with our lead asset, lacutamab, supported by partner 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. And the pool of preclinical projects, including our NK cell engager platform, which we will carefully select and bring forward…

Thank you, Mondher. On Slide 7, let me start with lacutamab. 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 the poor prognosis for which there are few therapeutic options at an advanced stage. On Slide 8, I just wanted to remind you of our development strategy for lacutamab and 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 US Fast Track designation EU prime designation last year. We were also looking to potentially expand past Sézary syndrome to mycosis fungoides, where we have encouraging preliminary data from our Phase 2 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 9, let me highlight the great progress we have made this year in our ongoing Phase 2 TELLOMAK study for Sézary syndrome and mycosis fungoides. In mycosis fungoides, firstly we moved the KIR3DL2 expressing Cohort from Stage 1 to Stage 2, clearing a pre-determined threshold before 50% of the Cohort was enrolled. The KIR3DL2 MF data was also presented at [indiscernible] 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 2 mycosis fungoides data in KIR3DL2 expressers.…

Thank you, Frédéric. Thanks to Joyson. So 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. Moving on to our clinical program, we expect to achieve a number of milestone over the next 18 months. As you've heard from Joyson, our Phase 2 TELLOMAK study for lacutamab continues to progress. And we expect to report potentially pivotal data into 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 2 COAST data at ESMO this Friday, which build 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 3 of the Phase 2 in head and neck cancer study, just in the combination of monalizumab with cetuximab and durvalumab in IO naive patient with advanced neck cancer. We are further advancing the adenosine pathway agents in the clinic, where we are starting a new Phase 1 trial for IPH5301, the anti-CD73 we look forward to data from the anti-CD39 IPH5201 due in 2022. In parallel, we continue to develop our ANKET technology platform and we are very encouraged by the preclinical results from our next-generation NK cell engagers. 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 of [indiscernible] cancer immunotherapy with more to come as Joyson said, this Saturday is an oral presentation at ESMO [indiscernible]. We…

[Operator Instructions] We're taking our first question from the line of Daina Graybosch. Please go ahead.

Hi. Thank you for the question. Two for me. One, just thinking ahead for the monalizumab data to be spin it on Saturday. I wonder if you could remind us how much overlap in efficacy and read through from concept to proof-of-concept study? Do you believe there is a new combine monalizumab with durvalumab versus cetuximab? Does either of these therapeutic combinations or mechanisms [technical difficulty] activities at CD8 cells or NK cell? And then in addition, keeping alive my [technical difficulty] could we see NeoCOAST data this half? I noticed it's not on your milestone slides, so maybe you don't have specific visibility, just wondering of the possibility [technical difficulty].

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. So you ask question on the NeoCOAST data, when this data will be public. And 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. AM I …

Correct.

… repeating correctly -- okay. Okay, perfect. So I will 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 side, which is that the data are expected in the second half of 2021. So we will hear more problems 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 the blockers in our labs. The first one is a way to enhance the [indiscernible] of antibodies that, like cetuximab could have a synergistic effect when combine it with monalizumab. And that's what led to the head and neck program and the Phase 3 trial that was started last year. And the second piece of information and piece of data that was published already in [indiscernible] in 2019 was basically the technical package that supported the clinical program of the combination of monalizumab, and anti-PD1 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. So, first of all, I think the two trials and the two setting and the two type of combination are supported by strong scientific rationale. Now, 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 presented and of course, I would be very cautious not to have cross trial comparisons or read across, but I'll hand over to Joyson who can maybe complete this answer.

Yes. So 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, that 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. And it would be hard to kind of read across the trials or read from across trial comparisons, not only because we try not to do that, but also just because of the differences of indications, settings as well as mechanisms of action.

Thank you, Joyson. Does it answer your question, Daina?

Thank you. Yes, it does. Thank you very much.

Thank you.

We are taking our next question from the line of Yigal Nochomovitz at Citigroup.

Thanks, Mondher. I just had a few questions. So first, I know obviously, you can't disclose the data yet on the ORR and PFS proposed ahead of the later-breaking presentation. But that said to the extent that you can comment generally, what percent improvement in ORR and PFS would you view as clinically meaningful benefit for monalizumab plus durvalumab combo over the durvalumab monotherapy? Thanks.

Thank you, Yigal. Again, we look forward to seeing the full data presented at ESMO as you know as an oral later-breaking abstract. This was detailed by [indiscernible] curtain raiser. They will report ORR, but they also present PFS data for both arms, durvalumab plus monalizumab and durvalumab plus [indiscernible]. I think the design of the trial is well-known. It has been already publicly disclosed. It's well controlled phase -- randomized Phase 2 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 patient who finished their chemo radiation therapy and are randomized within 6 weeks, if they do not progress. And they are being treated with durvalumab mono or durvalumab for up to 12 months. The response rate is certainly a very important endpoint and is the primary endpoint for this trial. But 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. So I believe the response rate is certainly important to assess and we look forward to seeing the data, but I think the PFS is something crucial to keep in mind.

Okay, got it. Thank you. And then 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 and Japan, there are only 200 Sézary patients and about 3,000 mycosis fungoides patients according to the [indiscernible] database.

Yes, 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 trials?

No, more about the commercial opportunity.

Yes, okay. Yes. Yes, thank you. No, I -- 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 express in KIR3DL2 and we have seen in the Phase 1 basically from the first dose level that when you target this, this tumor antigen KIR3DL2, you get significant tumor shrinkage and even improvement in quality of life. I think this is a symptom 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 recognition [ph] or brand recognition and exchange with the FDA and with EMA in order to accelerate the clinical development. The intent, of course, is to expand beyond that and the mycosis fungoides is half of the PTCL as you know. And you’re right, in mycosis fungoides account for about 3.5 to max 4,000 new patient every year in the U.S and in Europe and Japan. And about 4,000 non-mycosis fungoides peak cutaneous T cell lymphoma. So all in all, we're talking about up to 8,000 patients with cutaneous T cell lymphoma, half of them would express the KIR3DL2. And again, the mycosis fungoides segment is not the end of the story. It's certainly much more attractive and much more compelling business case. But of course the -- 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 [indiscernible] in T cell lymphoma, which express the KIR3DL2, which of course, surely define, if I may say the scientific rationale to expand now to [indiscernible] T cell lymphoma from where business [indiscernible] of course with more than 18,000 new case every year. KIR3DL2 [ph] T cell lymphoma has a much more attractive commercial prospect. But again the step-wise approach is to validate the mechanism of action, check that this is not the Sézary syndrome drug but it works outside Sézary syndrome which we are exploring and validating as we speak in lacutamab and then go with KIR3DL2 [ph] T cell lymphoma. And then when you look at the totality of the business case, it's no longer niche indication, it's a significant market opportunity.

Got it. Thanks. And just I had one final question. This one might be good for Eric or Joyson. I'm just curious about the ANKET platform and the course of combining NKp46, CD16 and IL-2R. So is the thought that this tetra-specific asset would be better suited to solid tumors or to hematologic malignancies, or both categories under consideration?

Yes. That's another excellent question. That, of course, we debate internally and I'll hand over to Joyson, to sum up the thoughts behind the selection of the tumor antigen for these multi-specific antibody. Joyson?

Yes, thanks, Yigal, for the question. So, yes, I mean -- so I'm going to kind of go back and talk a little bit about the ANKET platform. And the amazing thing about the ANKET platform is it's very versatile. So as you were stating the NKp46 CD16 attachments to the NK cells with the IL-2 variant in the same. But the tumor antigen is what I call as removable. You could kind of put different tumor antigens in there. This allows for that flexibility. And as Mondher 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. So 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. [Operator Instructions] 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 5301. Certainly will be interested to see what the lacutamab data is for the AstraZeneca compound. But could you remind us how to think about differences that you are aware of between their asset and your assets? That's my first question around 5301. And then 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 lacutamab. So that's the second question. And then 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. So how is the company thinking about financing options? What kind of options are available and what's the strategy? Thanks.

Thank you, Graig. Very, very important and good questions as usual. I will start with the first one. Then hand over to Joyson for the COAST and the mechanistic approach we are thinking about, in particular, with regard to the potential combination with [indiscernible] CD73. And then I'll give the opportunity to our new CFO, Frédéric to address your question about the financing moving forward. Very briefly on the 5301. So as you said, I mean, we do really look forward to seeing the lacutamab data. I remind you, other than those data actually, I'm not aware -- we are not aware of other public randomized data in this field. Everyone remember the BMS and DAG [ph] Phase 1b data presented about 2 years ago at ASCO and AACR showing some trend of activity, but nothing since then. So clearly, the results of the COAST trial with regard to lacutamab 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 the data. And again, we have even presented with data at AACR back in 2019, if my memory is correct, comparing our anti-CD73 with the BMS and the [indiscernible]. And 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 trial into clinical benefit for patient and that's why we were, to some extent, waiting to see, some very data [indiscernible] in order to try to learn from others. And 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 anti-CD73. That's my answer for your first question. Now, Joyson, the question around COAST. How do we think to the extent across -- I don't want to speculate of the data, but the mechanism of action and the potential convenient compatibility with an anti-CD73 if the two arms are affected?

Yes. So I think I'll go back and kind of also state that the mechanisms of action here clearly are as we know are different. So one is an anti-CD73 and anti-NKG2A. One, we're looking to see, I mean, we have preclinical data that have supported ADCC synergy. And then finally with monalizumab, it's sort of done redundant pathway, mechanism of action in combination. So I think when we look at this, we see two, once again, two different tumor types, I mean, two different -- I mean same setting, but 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. But I would just say these are two very distinct mechanism of actions operating in two different ways. One, sort of -- sorry, both of them relieving immune suppression. And so I just messed up the cetuximab question, but this was CD73. So the CD73, it's basically the [indiscernible] of the tumor, the amount of adenosine that's present. So really decreasing immune suppression. So decreasing adenosine is one. The other one is decreasing in two different pathways, one anti-NKG2A and the other one with PD1. So I think with that, we'd have to wait for the clinical data to see what's happening.

Thank you.

I know that was a little roundabout, messed up answer. So I'm happy to repeat it. Because I think it might have I had cetuximab, and then I was like, oh, gosh, this isnt cetuximab. So clearly, I'm excited about both of these. And I'm like sitting here going okay, but -- yes, so, in short, the CD73 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. And so I think the clinical data will speak for at least which pathway be better. I think that last answer is the one I would kind of coin versus my first.

Okay. Thank you, Joyson. Thank you. Thank you. Frédéric, would you want to take the question on what's the plan and the financing of the company moving forward? Frédéric Lombard: Yes. Thank you, Mondher. Yes, as I said before, the cash position is quite robust at the moment with €159 million. We constantly monitor our financial needs, and 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, but it's not following a disinvestment on the outside, 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. So 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.

And then just in terms of how you're thinking about potential options to extend the cash runway? Frédéric Lombard: The -- at the moment, first of all, we -- Mondher, you wanted to?

No, no, please, please go ahead. Frédéric Lombard: Yes, okay. So the different options are, we look at the markets, for sure. We look at financing options also with some banks as well. But more than ever, we look at progressing the way we operate, and see what we can get out of those partnerships.

Yes. So, Graig, long story short, we have a solid cash position. And we've been actually -- 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 provide an update when needed. Thank you.

Okay, thank you.

Operator, do we have more question on the line?

Yes, we have one question from [indiscernible]. Please go ahead. Your line is open.

Hi. Good morning.

Hey, good afternoon, Mondher and greetings to the gentlemen Thanks for taking my question. So I just wonder one question on the monalizumab for the data is going to be reported for the IO naive patients later this year. So could you remind us what kind of data set we could expect? And like how many patients we could look into the data? Thank you.

Yes. Joyson, would you like to answer or I can take it. Okay.

No, go -- yes, go ahead Mondher.

Go ahead. Yes. Okay. Thanks [indiscernible] for the question. So, first of all, to remind everyone, this is a single arm study that tests the triplet combination. And again, we, as I said in my answer to the first question, we have this 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 synergistically an anti-PD-L1. And because data were built 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. So this study was designed really first of all to assess the safety of the triplet because this -- a reminder, this is the first I believe ever triplet are you to be the [indiscernible] triplet of noncytotoxic or chemo free regimen to be [indiscernible] in head and neck cancer. The safety was good with the first 20 patients. So we extended the trial to 40 patient, but yet still single-arm trial in advancing relapsed or metastatic patient with squamous cell carcinoma of the head and neck who might have been pretreated with chemotherapy or radiation therapy but who are made of any [indiscernible] treatment. The data will be presented at the end of the year, and we are looking at the totality of the data [indiscernible] to really determine what's the platform. As you know the competitive landscape is evolving and it's important to take into consideration and see the specific unmet need and where we can position this triplet. And again, I insist on the fact that today the standard of care is [indiscernible] plus or minus chemo dependent on the level of CPS and the reserves that we are presented 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 and we will be delighted to share this data as I said towards the end of the year.

Thank you for that and congratulations on the progress.

Thank you very much. Thank you. Operator?

Thank you. There are no further question on the phone.

Okay. Henry, do we have questions on the webcast?

No more questions, Mondher. Thank you.

Okay. So if there are no more question, 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 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. You may all disconnect.

Thank you. Bye, bye.