Innate Pharma S.A. (NASDAQ:IPHA) Q3 2022 Earnings Call Transcript

Innate Pharma S.A. (NASDAQ:IPHA) Q3 2022 Earnings Call Transcript November 14, 2022

Operator: Hello, and thank you for standing by. My name is Regina and I will be your conference operator today. At this time I would like to welcome everyone to the Innate Pharma publication of revenue for Third Quarter 2022 Conference Call. All lines have been placed on mute to prevent any background noise. After the speakers’ remarks there will be a question-and-answer session. I would now like to turn the conference over to Henry Wheeler, Head of Investor Relations. Please go ahead.

Henry Wheeler: Thank you. Good morning. Good afternoon. And welcome everyone. This morning, Innate issued a press release providing a business update for our Q3 2022 results. We look forward to highlighting the progress made during the quarter as well as addressing future goals and milestones. The press release and today’s presentation are both available on the IR section of the website. On Slide 2, before we start, I would like to remind you that we will make forward-looking statements regarding the financial outlook in addition to regulatory and product plan developments. These statements are subject to risks and uncertainties that may cause actual results to differ from those forecasted. On Slide 3, on today’s call, you will see we will be joined by Mondher Mahjoubi, our Chief Executive Officer; who will then hand over to Joyson Karakunnel, EVP and Chief Medical Officer; and then Yannis Morel, EVP of Business Development and Product Portfolio Strategy.

We will also have our CFO, Frederic Lombard, on the line for Q&A. Mondher, I’ll now hand the call over to you.

Mondher Mahjoubi: Thank you, Henry. Good morning. Good afternoon everyone and thank you for joining our call today. Please move to Slide 4. And let me start by reminding you our strategy. Our strategy centers around three key priorities where we look to derive value from our early R&D effort through later stage partnerships, where it makes sense to do so. Firstly, we look to create near-term value driven by our lead proprietary product candidate, lacutamab, which is in development for T-cell lymphoma, with readouts in PTCL happening in the second half of this year, and two trials in the larger indication of peripheral T-cell lymphoma underway. Second, we continue to shoot our pipeline and create longer term value by leveraging our antibody engineering capabilities to develop innovative molecules with a primary focus on our multi-specific NK cell engager proprietary platform called ANKET.

Sanofi has the most advanced ANKET in the clinic and have selected another candidate and we are nearing the clinic with the others, notably, with our CD20 targeted tetra-specific ANKET called IPH6501. Last but not least, we are building a strong and sustainable foundation for our business leveraging various partnerships across industry and academia. Here, our AstraZeneca partnership with monalizumab, which is continuing in lung cancer and our focus remains to leverage the value of our products as much as possible. We want to ensure that if we can gain valuable competencies via a partner agreement, we will consider that in our development plans for the product. These will further validate our science and offer capital that we can reinvest to advance our early portfolio.

Before I hand over to Joyson, please move to Slide 5. Slide 5 is an overview of our pipeline, which shows how we continue to translate our science into a robust portfolio of proprietary and partnered assets. It also illustrates how we are executing against our strategy with our lead proprietary asset, lacutamab, supported by partnered and earlier stage product, in particular from our NK cell engager ANKET platform. We anticipate a number of potential clinical readouts and catalysts in the upcoming couple of years as our R&D engine looks to leverage our scientific know-how to create a sustainable business. I would like now to pass the call over to Joyson, who will review the progress made with our portfolio, starting with lacutamab, our most advanced proprietary asset.

Joyson, over to you.

Joyson Karakunnel: Thank you, Mondher. On Slide 6, let me start with 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. In the TELLOMAK trial, Cohort 1, including Sézary syndrome patients, could potentially be a pivotal cohort. We announced that we will present preliminary data from this cohort at the ASH Annual Congress in December. For mycosis fungoides, we have cohorts 2 and 3 where we are testing the hypothesis of non-expressors and expressors of KIR3DL2 using the frozen companion diagnostic assay. In September, we presented preliminary data from the mycosis fungoides Cohort 2 at the EORTC Congress in Madrid.

Slide 7 summarizes the preliminary Cohort 2 and 3 data in mycosis fungoides presented at EORTC in September. As a reminder from the data presented last year as expected, our scientific hypothesis confirmed in Cohort 2 high global response rates in comparison to the benchmark and the non-expressive cohort, a low global response rate in the non-expressing cohort. At the EORTC Congress this year at the presentation in the KIR3DL2 expressing Cohort 2, we were encouraged to see that in these late-line patients with a median of four prior treatments, lacutamab demonstrated a 28.6% ORR and six responses. We are particularly encouraged by the responses in the skin where we saw a 57.1% ORR and 12 responses. On Slide 8, we have the abstract published on the ASH Annual Congress 2022 website ahead of the Congress in publication of the data in December.

The abstract details that in this heavily pre-treated post-mogamulizumab patient pool with the median prior line of therapy of six and 10.9 months of median follow-up, the ORR in the ITT population was 21.6%, with an ORR of 35.1% in the skin and 37.8% in the blood. A favorable safety profile was mentioned. We look forward to discussing the data in more detail after the presentation at the ASH Annual Congress. On Slide 9, let me summarize the progress we are making with lacutamab. We are pursuing a fast to market strategy for lacutamab in the niche setting of Sézary syndrome where lacutamab was granted U.S. Fast Track designation and EU prime designation in 2020. We have expanded past Sézary syndrome to mycosis fungoides, where we have seen encouraging preliminary data from our Phase 2 trial in both cohorts.

For the Sézary syndrome and mycosis fungoides enrollment is on track with final data due in 2023. Finally, we are continuing to enroll into peripheral T-cell lymphoma in the monotherapy and combination trials in the relapse setting. On Slide 10, I would like to update you on monalizumab, to remind you monalizumab is anti-NKG2A which acts upon the checkpoint pathway to potentiate NK cell activation that we have licensed to AstraZeneca for oncology. On this Slide you can see an overview of the late stage development plan for monalizumab in lung cancer. Based on the AstraZeneca sponsor Phase 2 COAST data, AstraZeneca commenced PACIFIC-9. A Phase 3 trial evaluating the combinations of either monalizumab or lacutamab plus durvalumab in the un-resectable Stage 3 non-small cell lung cancer spending who have not progressed after concurrent chemo radiation therapy.

For the Phase 2 COAST study, the RRR’s evaluated the combinations of durvalumab plus monalizumab and durvalumab plus oleclumab. AstraZeneca is anti-CD73. As published in the Journal of Clinical Oncology by AstraZeneca immediate follow up of 11.5 months. The results of an interim analysis showed a hazard ratio of 0.42 under for durvalumab plus monalizumab versus durvalumab alone. These results also showed an increase in the primary endpoint of confirmed ORR for durvalumab plus monalizumab overdue value alone of 36% versus 18% respectably. We look forward to further updates from this study for AstraZeneca. I will now hand over to Yannis to cover our NCAP program.

Yannis Morel: Thank you, Joyson. On Slide 11, I wanted to highlight our proprietary multi-specific NK cell engager platform that we call ANKET. ANKET standing for Antibody-based NK cell Engager Therapeutics. ANKET is a versatile, fit-forpurpose technology made of various reading blocks that is creating an entirely new class of tri- and tetra-specific engager to induce synthetic immunity against cancer. This technology platform, which is leveraging our scientific expertise in the NK cell space, will be an enzyme for our pipeline creating value via multiple drug candidates addressing multiple tumor target. The backbone of this ANKET platform is based on the unique engagement of the activating NK cell receptor NKp46 and CD16 on the NK cells, which allows for optimal harnessing of the NK cell effector function, which can be further increase by addition of either two variant that induce their poliferation.

On Slide 12, I wanted to share with you why we are so excited for this platform and why there is a growing interest from the industry in the NK cell space. As you can see on the left part of the slide on the PET scan image published by the group of a pioneer work using adaptive sensory NK cells as provided proof of concept that NK cells can induces strong antitumoral response. That’s exactly what we are aiming to replicate with our ANKET molecules, which are designed to engage efficiently in the NK cells of the patient behind the tumor. In the middle panel, you can see the detailed mechanism of action of the tetra-specific ANKET molecule. On one end the engagement of the activating NK cell receptor NKp46 and CD16 on NK cells triggers antigen dependent killing of the tumor, as well as production of key cytokines for the anti-tumoral immune response.

On the other end, the addition of IL-2 variant, which target the IL-2 receptor beta gamma complex on NK cells in use, NK cell proliferation within the tumor micro environment increasing therefore the number of anti-tumor effector cells. Overall, this platform demonstrates comparing in clinical antigen efficacy as evidenced by the strong efficacy that you can see on the green path. Lastly, on the right you can see our growing pipeline of ANKET molecule with Sanofi having licensed two molecules, which I will cover in the next slide. Our most advanced proprietary ANKET is a tetraspecific molecule targeting CD20 and code IPH6501 for which we plan to file an IND next year. We also have other able targets for which we ought to provide some updates on new course.

On Slide 13, you can see our most advanced ANKET program is a CD123 targeted high-specific molecule called IPH6101 or SAR’579 that we have generated in collaboration with Sanofi. It is now licensed to them and currently in Phase 1 trial. We also announced over the summer that Sanofi Prosodie keeps the further development to second drug candidate. It is IPH6401 of SAR’514, which is BCMA-targeted tri-specific ANKET molecule, which is using Sanofi Prosodie molecular formats, which shows the versatility of our platform. We have announced €30 million in milestone to date from this partnership. On Slide 14, we are pleased to have a few presentation at ASH, like in the development of lacutamab as well as several updates for the ANKET platform. This includes a two program with our partner Sanofi and our presentation from our CSO, Eric Vivier who will present the ANKET platform including our latest update published last month in Cell Reports Medicine.

We will have also update at the ESMO IO conference in December for our anti-CD39 program called IPH5201. I will now turn to Mondher for a summary of the catalyst and close.

Mondher Mahjoubi: Thank you, Yannis. Please move to Slide 15. As you can see we are working diligently to execute across all our strategic pillars, and we believe that we are laying the foundation to drive near and long-term value. Looking at our clinical program, we expect to achieve a number of milestones over the next two years. First, as you’ve heard from Joyson, our Phase 2 TELLOMAK 34 lacutamab continues to progress. We have reported preliminary data this year, with final data due next year. In addition, our Peripheral T Cell Lymphoma program initial data are expected next year. For monalizumab the lung cancer trial are in the way and we continue to advance the adenosine pathway agents in the clinic where we look forward to sharing our Phase 2 plans in due course.

In parallel, we continue to develop our ANKET technology platform including with our partner Sanofi, and we are very encouraged by the preclinical results from our next generation NK cell engages. We believe that this represents a natural evolution of our platform with data presented at conferences at the end of the year. Finally, we look forward to further update on our proprietary ANKET IPH6501 as you’ve heard with the IND on track to be filed next year. Let’s now move to the conclusion slide. Lastly, on Slide 16, as you can tell, we continue our exciting journey at net. We look to build our business to create value for patients and stakeholders. And in summary, we have positioned Innate Pharma for the future with our strategy and made meaningful progress throughout the year-to-date across all three strategic pillars.

We have carefully managed our resources so we can continue to invest in progress in our pipeline. And I am very pleased that we continue to have a strong cash position with a runway into the second half of 2024 with $151 million as of September 30, 2022. Collectively, we are driving value across our business and ultimately advancing our goal to deliver innovative medicine to patents. We look forward to keeping you updated on our progress. This concludes our prepared remarks. We will now open the call to questions.

Q&A Session

Operator: Our first question will come from the line of Yigal Nochomovitz with Citigroup. Please go ahead.

Yigal Nochomovitz: Hi Mondher and team. Thank you very much for taking the question. I just had two; one on TELLOMAK and then one on the tetra-specific ANKET. So on TELLOMAK, I was just interested in the Cohort 3, which I know is the one with the non-expressor. You still had some good responses albeit not all of them characterized as TRs. I was just curious that because those patients are still expressing some low level of the target KIR3DL2 or is there another reason? And then on the tetra-specific ANKET, obviously CD20 is a very well known target, so I’m assuming the idea there is to pick something that’s very well validated so that you can show what the tetra-specific platform can do above and beyond the known target as opposed to introducing a totally new variable in addition to the tetra-specific ANKET. So if you could just elaborate on your thinking there? Thank you.

Mondher Mahjoubi: Thank you, Yigal for the two very important questions. Actually, we’ll start with the second one and I’m going to hand over to Yannis who set-up €“ set the context actually of the identification and selection of this target. And then Joyson will address your question about the level of activity we have seen with Cohort 3, you’re absolutely correct we €“ it’s not nil, it’s not zero. We have some activity and we have some hypothesis to explain actually that level of activities. But let’s start with the ANKET platform and the CD21st.

Yannis Morel: Yes. Hi Yigal, Yannis speaking.

Yigal Nochomovitz: Hi.

Yannis Morel: I think you’re right. We selected CD20 in order to limit the number of variables where with this new tetra-specific molecule we are really progressing to the clinic. One new mechanism of action relied by €“ relying on the activations NKp46 and 16, as well as the cytokine in the same molecule. So as we’re bringing this for the first time into the clinic, we decided to go after a very well validated target, and CD20 is obviously one of these, and which is also the advantage when you look at the expression as opposed to other potential validated targets to be quite stable cause a different line of treatment, meaning that if you have like lacutamab relapse patients lot of them are still expecting the target, which basically from our perspective the ideal candidate for this proprietary program in the clinic. That way we have also others at the preclinical stage with other targets.

Mondher Mahjoubi: Thank you, Yannis. And without of course adding too much as you have seen in data we have already presented. We believe that we have really differentiated asset based, at least on the safety profile generated so far, but also on the pre-clinical antitumor activity that we have published in various tumor model. May I ask Joyson maybe to address your question on why we still have responses in Cohort 3 despite the fact that there are two level of expression is below the 1% to short.

Joyson Karakunnel: Yes. So just as a reminder, I mean, the Cohort 3 is mycosis fungoides in Cohort 2s the expressing mycosis fungoides, Yigal as you mentioned. Now there are different factors. One is of course the heterogeneity. Tumor is number two is the assay sort of assays conditions. So because of those two, we do see some low levels of activity even in the non-expressors. Now, we’re further exploring this also to both make our assay more precise by looking at an all commerce cohort. So keep in mind the TELLOMAK study does have a commerce cohort also, which will be looking at the FFPE assay we’re keeping in mind that Cohort 2 and Cohort 3 were a based assay. So these are sort of the reasons why we believe that you’re seeing some low level activity.

Yigal Nochomovitz: Got it. Thank you.

Mondher Mahjoubi: Thank you.

Operator: Your next question will come from the line of Daina Graybosch with SVB Securities. Please go ahead.

Daina Graybosch: Hi. Thank you for the question. Two for me on TELLOMAK and lacutamab. I wonder if you can talk about what you think are regulatory expectations for accelerated approval, whether in these diseases they focus on the global response rate or whether the skin or blood response rates are used in their regulatory review? And then the second question is, as we’ve all been hearing a lot more about project OPTIMUS, I wonder if you could remind us if you’ve done any randomized dose optimization between two doses of lacutamab, and if not, how you plan to do that to meet the loose project OPTIMUS €“ I don’t know, let’s say guidelines, but almost guidelines from FDA? Thank you.

Mondher Mahjoubi: Thank you, Daina, for two very important question. I think Joyson is probably the right person to address, first of all our, our thinking about the accelerated approval of lacutamab in Sezary syndrome, and of course the evolution of the regulatory environment in the U.S. Joyson?

Joyson Karakunnel: So, sure. So in regards to the regulatory sort of benchmark or what the regulators may be looking for, we’re in ongoing discussions with them certainly. So at least at this point in time I want to say what they’re considering for accelerated approval, of course, as we know this, this benchmark is €“ this for accelerated approval has become a bit tougher in the last few months or so just because of the scrutiny that’s been put on the accelerated approval program at the FDA. I think number two is in regards to project OPTIMUS, interestingly project OPTIMUS is just dose justification. And for us dose justification we have looked at dose justification and continue to ensure that going forward the dose is correctly justified.

So I think we’ve been doing this for drug development for years on end and, I think lacutamab it has been done accordingly. I don’t believe that the FDA has guided that you must do a randomized trial, but instead they do say to explore several different doses at different levels, and it’s not necessarily based on randomization with the statistical significance.

Daina Graybosch: Can I have a follow up? Can you remind us?

Joyson Karakunnel: Daina, does that answer the question?

Daina Graybosch: Yes. Can you just remind us because it happened longer ago, how many doses you explored and sort of how many patients at various doses?

Joyson Karakunnel: So we did explore several different doses. We explored both intra €“ hello? Hello. Did I just get cut off?

Daina Graybosch: Joyson, I can still hear.

Joyson Karakunnel: Well, okay, okay. I don’t know if I got cut off. So we did explore several different doses, both intra patient dosing as well as patients who received a single dose throughout. So we do have several different doses with adequate number of patients and doses at least that we were able to look at some of the PK and PD?

Daina Graybosch: Thank you.

Mondher Mahjoubi: Daina, if you want you can follow-up and maybe send you the Phase 1 data that we published, as you know, in New England a couple of years ago, where we have the detail escalation, okay.

Daina Graybosch: Yes, sorry, .

Mondher Mahjoubi: Yes. Thank you.

Operator: Your next question will come from the line of Swayampakula Ramakanth with HCW. Please go ahead.

Swayampakula Ramakanth: Thank you. This is RK from HCW. Couple of quick questions on the €“ on the TELLOMAK trial we know that you went to present some initial data on the Sezary syndrome at ASH, but what’s the expectation for the final results of this €“ of the TELLOMAK trial itself? And also for the same drug, can you highlight a little bit about, your work with PTCL? That would be helpful. Thank you.

Mondher Mahjoubi: Hi. RK, let me thank you. We definitely thank you for the question. Let me repeat them just to make sure we got them right. So, first one is about the data to be presented at ash and in particular what expectation we have with regard to the level of activity for lacutamab in Sezary syndrome, in other words, sort of targeted product profile? And the second question is an update on the PTCL, and once again actually Joyson is the right person to address both questions. Joyson, back to you. You’re mute, Joyson.

Joyson Karakunnel: I didn’t €“ sorry, I didn’t hear the PTCL question, but let me go ahead and address the Sezary syndrome question first. So in Sezary syndrome, just from the abstract that was published for ASH, we did have a global €“ just as a reminder, this was a very heavily pretreated population who were postpone to monalizumab with a median number of six lines of therapy. And with that, we had seen a global confirmed ORR of overall response rate of 21.6%. So we were very encouraged by that, and we do expect that we would continue to see encouraging data even in the final data set itself. And I’m sorry, what was the PTCL question?

Mondher Mahjoubi: I will take the PTCL 1, so just too maybe make sure I got to try. Okay, you were asking for an update on the PTCL, and as we have two trials in peripheral T-cell lymphoma, a company around Phase 1b trial assessing the level of activity and the safety of lacutamab in monotherapy. And we have a LYSA sponsored trial. LYSA is a European cooperative group well known in HEM that is testing the combination of lacutamab with chemotherapy, in particular with the combination of GEMOX. And we said that at the previous call that an interim or preliminary data will be presented in 2023; so next year.

Swayampakula Ramakanth: Thank you. Thanks for taking the questions.

Mondher Mahjoubi: No questions on the line. If not, I’ll go to offline submitted questions.

Operator: No further phone questions at this time.

Henry Wheeler: Okay. So we have a question here from Olga Smolentseva at Bryan Garnier. Three parts to the question. Firstly, could you give us any favor what we should expect from the Phase 1 data for IPH5201 at ESMO IO? And do you see any read across for IPH5201 from the recent polls of an anti-CD 39 program by Surface Oncology?

Mondher Mahjoubi:

.:

Henry Wheeler: Thank you. Second question from Olga. How do you see IPH6501 fit into the highly competitive landscape of CD20 targeting bi-specifics?

Mondher Mahjoubi: Yes, another important question. I think Yigal, I believe, asked a question along the same line. We are fully aware of the, of course, competitive landscape here, but as Yannis said we will further evaluate this landscape as we enter IND filing next year. And we’ll provide an update on the exact indication that we are pursuing. But from what we have seen in the technical data so far, there is really an opportunity here to differentiate IPH65, both on safety, but on improved efficacy. I must also say that this is again the first proprietary tetra-specific ANKET molecule enter into the clinic. And the selection of validated target was a way to mitigate the risk of going after completely novel platform, which is the tetra-specific. So that was our approach to really mitigate the risk of the novel platform by choosing well, established and validated target.

Henry Wheeler: Thank you. And last question from Olga. Should we expect the final data for lacutamab in Sézary syndrome to include a similar highly pretreated patient population as per the interim update at ASH?

Mondher Mahjoubi: Yes. Again, I think, I may be stating the obvious, but patients in this trial needed to have at least two lines of prior therapy and must be post-moga. As you may remember, as moga was still in the launching phase, and some of the reason when we started the trial, patient ended up being very late line, and no reason to think that the rest of the trial would be any different. So we continue to enroll according to our inclusion/exclusion criteria, i.e. STAGE IVA and STAGE IVB relapsed/refractory, two or more prior line of systemic therapy, including mogamulizumab. These are the main selection criteria. And despite having a median of six line of prior systemic therapy, we are encouraged by the top line ASH abstract efficacy and we look forward to discussing this data further at the ASH presentation. Final data, as I said earlier, are due in 2023 for both our mycosis fungoides and Sezary syndrome cohort.

Operator:

Henry Wheeler: Thank you. We have a couple more questions submitted on online. So Jingming Chen at Evercore. Submitted a question to before, do you plan to file for approval in SS first or wait to do a trial studying MF and SS combined? What are the main matrix considerations for the decision?

Mondher Mahjoubi: Yes, I’m going handover back to Joyson to recap our strategy in terms of development and agitation for lacutamab in Sézary MF. Joyson?

Joyson Karakunnel: Thanks, Mondher. So I think to answer your question, do we plan to file for approval in SS first or wait to do trial studying MF and SS combined, I think, number one is this is going to depend a lot on the data, so we are keeping all our options open. That includes the potential to file for SS first. That also includes the potential to file for both all during that time, of course, considering even partners in the mix. So just kind of making sure all our options are open and what are the main matrix and considerations for this decision. Number one is, is the data itself will drive the decision. So, the strength of the data will drive the decision. Number two is, is sort of the regulatory landscape as it starts to evolve, we’ll have a major influence on how we look at this. And then third is our ability to look for a partner.

Henry Wheeler: Thank you, Joyson. I have some further questions submitted online. So Eric Berrigaud at Stifel. Question one, lacutamab has delivered consecutively two highly confirming sets of data in MF and SS. Now, many times in the past you explained the ability of lacutamab to find a good partner would be heavily dependent on the interim data in PTCL. This is, however, quite speculative at this stage. Therefore, how should we think of both the value and the future of the compound if PTCL does not deliver on promises? In other words, how much dependent upon PTCL is the future of lacutamab overall?

Joyson Karakunnel: Thank you Eric for a very important question. I would say, first of all, we follow the science and of course we will define what is the right thing to do based on the data at hand. You are well aware, of course, the business case in Sézary and also the potential in in MF. And clearly having a PTCL indication would completely change the perspective of this drug moving from maybe just few hundred million to blockbuster PTCL is there. I think at this point in time we need to validate the signal through TELLOMAK trial and the preliminary data we have so far in the abstract that is submitted to ASH is going into the right direction. I think we’ll wait for the PTL data to emerge, at least the preliminary data next year to assess the various scenario.

But keep in mind that we have two shots, if I may say, at goal. We have a monotherapy trial, which is maybe a high risk, but nevertheless, I think, an opportunity to identify single agent activity in a heavily pretreated and difficult to treat patient population. And we have also the combination trial with the LYSA group, which of course, another way to explore the potential of lacutamab in this disease. And of course, these are the not only option that we are thinking of there are many other opportunity in second line, but also in frontline that are being explored by the team. But I think it’s important that we generate the first set of data to better understand actually how to position and to deliver value for this asset.

Henry Wheeler: Thank you. Second question from Eric. In TELLOMAK patients are required to be pre-treated with moga, you collected very advanced patients on average with six previous lines of treatments. As time progresses is it fair to say that moga is now used earlier and therefore that you would treat less advanced patients if approved?

Joyson Karakunnel: Again, I think it’s an important question. And similar to what I said earlier it’s difficult to speculate on the €“ I’ll say how heavily pre-treated are on the patient that will be recruited in the next couple of months. But as I said moga was still in the launching phase and even after launch moga did not get reimbursed everywhere. So, we had clearly in some region, wait when the drug was available. And we ended up, of course, recruiting patient with very late line of therapy. And we didn’t see a major change in, I would say, the access to mogamulizumab in some part of the world, at least in Europe. So there is no reason to think that the rest of the trial would be any different, and we may end up with yes, heavily pretreated and median of six line of therapy.

I think what is important is: a) validate that we have an activity and a meaningful activity in patient who have been exposed to mogamulizumab. That’s, I think, number one. And number two, of course, this is an area of n mathematically because by design in the post-moga setting there is no established standard of care. And of course, the data we generate with TELLOMAK would be of importance and, of course, will be discussed with the health authority when we have that.

Henry Wheeler: Thank you. Last question from Eric. Considering your previous comments on stability of the CD20 targets, would it be fair to expect your drug to go first in a very advanced line of treatment once existing CD20 antibodies have failed?

Yannis Morel: Yes, thank you, Eric for your question. Yes, indeed like I mentioned, your CD20 target antigen is pretty stable across the different line of treatment, including the monoclonal antibodies, but also other now T-cell engagers. You know that they are also in this type of NHL , but there are other targeting CD19. So I think that what you are saying is a pretty fair assumption that we can first start with the advanced line of treatment because we are mobilizing a very different mechanism of action as the current approved treatment like monoclonal antibodies or CAR T, but also the one that are in the Phase 3 and late stage development like NK cell engagers.

Henry Wheeler: Thank you, Yannis. I think we have no more question online. So I would like maybe as a concluding remarks remind you that as you have seen we continue to execute against our strategic priority. We have a strong financial position. We are well-funded into the second half of 2024. As we reported, also reads out from our proprietary and partnered portfolio program these readouts set the stage for delivering both near- and long-term value, while also highlighting the strength and depth of our core R&D efforts. And finally, looking ahead, we’ll continue to advance lacutamab program, move our early-stage R&D activity in the clinic with our next generation ANKET platform, while for monalizumab, we look forward to further clinical development in early lung cancer with trial with AstraZeneca underway, which further enforces of course, our strategy of building a sustainable business with robust R&D engine.

With that said, I thank you very much. Wish a wonderful day. Thank you.

Operator: Ladies and gentlemen, that will conclude today’s meeting. We thank you all for joining. You may now disconnect.