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spk09: 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 speaker's remarks, there will be a question and answer session. If you'd like to ask a question during this time, simply press star then the number one on your telephone keypad. If you would like to withdraw your question, press star 1 again. I would now like to turn the conference over to Henry Wheeler, Head of Investor Relations. Please go ahead.
spk00: Thank you. Good morning, good afternoon, and welcome everyone. This morning, Enate 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 two, before we start, I'd 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 risk and uncertainties that may cause actual results to differ from those forecasted. On slide three, on today's call, you'll see we will be joined by Monda Majubi, our Chief Executive Officer, who will then hand over to Joyce and Cara Connell, EVP and Chief Medical Officer, and then Yanis Morel, EVP of Business Development and Product Portfolio Strategy. We will also have our CFO, Frederick Lombard, on the line for Q&A. Monda, I'll now hand the call over to you.
spk06: Thank you, Henry. Good morning. Good afternoon, everyone, and thank you for joining our call today. Please move to slide four, and let me start by reminding you our strategies. Our strategy centers around three key priorities where we look to drive value from our early R&D efforts through later stage partnerships. Well, it makes sense to do so. Firstly, we look to create near-term value driven by our lead proprietary product candidate, Lakutamab, which is in development for TCN Informa with readouts in CTCL 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 NK. Sanofi has the most advanced NK in the clinic and has selected another candidate. And we are nearing the clinic with the others, notably with our CD20-targeting tetraspecific encode called APH6501. 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 Monolizumab, which is continuing in Lancaster. 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 products. This will further validate our science and offer capital that we can reinvest to advance our early portfolio. Before I hand over to Joyce, please move to slide five. On slide five is an overview of our pipeline, which shows how we continue to translate our size into a robust portfolio of proprietary and partnered assets. It also illustrates how we are executing against our strategy with our lead proprietary asset, like Hitamart, supported by partnered and earlier stage products, in particular from our NK-Cell Engager Unket 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 Jason, who will review the progress made with our portfolio, starting with lacudamab, our most advanced proprietary asset. Jason, over to you.
spk03: Thank you, Mandir. On slide six, let me start with our first-in-class humanized monoclonal antibody, that targets the immune receptor QR3DL2. As you remember, QR3DL2 is an inhibitory receptor found in approximately 65% of patients across all cutaneous T-cell lymphomas. In the TELEMAC trial, cohort one recruiting cesarean 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 mycoses fungoides, we have cohorts 2 and 3 where we are testing the hypothesis of non-expressors and expressors of CURE3DL2 using the frozen companion diagnostic assay. In September, we presented preliminary data from the mycoses fungoides cohort 2 at the EORTC Congress in Madrid. Slide 7. summarizes the preliminary cohort two and three data in mycoses fungoides presented at EORTC in September. As a reminder, from the data presented last year, as expected, our scientific hypothesis confirmed in cohort two high global response rates in comparison to the benchmark, and the non-expressing cohort a low global response rate in the non-expressing cohort. At the EORTC Congress this year, at the presentation in the Cure3DL2 Expressing cohort. Two, we were encouraged to see that in these late-line patients with a median of four prior treatments, lacudimab 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 eight, We have the abstract published on the ASH Annual Congress 2022 website ahead of the Congress and publication of the data in December. The abstract details that in this heavily pre-appreciated post-MOGA enolizumab 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 is mentioned. We look forward to discussing the data in more detail after the presentation at the ASH Annual Congress. On slide nine, let me summarize the progress we are making with lacudimab. We are pursuing a fast-to-market strategy for lacudimab in the niche setting of cesarean syndrome, where lacudimab was granted U.S. fast-track designation and EU prime designation in 2020. We have expanded past cesarean syndrome to mycosis fungoides, where we have seen encouraging preliminary data from our phase two trial in both cohorts. For the cesarean syndrome and mycosis fungoides, enrollment is on track with final data due in 2023. Finally, we are continuing to enroll in peripheral T cell lymphoma in the monetary fee and combination trials in the relapse setting. On slide 10, I would like to update you on monolizumab. To remind you, monolizumab is an 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 monolizumab in lung cancer. Based on the AstraZeneca-sponsored Phase 2 COST data, AstraZeneca commenced Pacific 9, a Phase 3 trial, evaluating the combinations of either monolizumab or aliquilumab plus durvalumab in the unresectable Stage 3 non-small-cell lung cancer study, who have not progressed after concurrent chemoradiation therapy. For the Phase 2 COST study, the three arms evaluated the combinations of Dervalumab plus Monolizumab and Dervalumab plus Oliculamab, AstraZeneca's anti-CD73. As published in the Journal of Clinical Oncology by AstraZeneca, after a median follow-up of 11.5 months, the results of an interim analysis showed a hazard ratio of 0.42 for Dervalumab plus Monolizumab versus Dervalumab alone. These results also showed an increase in the primary endpoint to confirmed ORR for Dervalumab plus Monalizumab over Dervalumab alone of 36% versus 18% respectively. We look forward to further updates from this study from AstraZeneca. I will now hand over to Yanis to cover our NCAT platform.
spk05: Thank you, Joyce. On slide 11, I wanted to highlight our proprietary multispecific NK cell engager platform that we call NCAT. NCAT standing for antibody-based NK cell engager therapy. N-CAT is a versatile, fit-for-purpose technology made of various building blocks that is creating an entirely new class of tri- and tetra-specific engagers to induce synthetic immunity against cancer. This technology platform, which is leveraging our scientific expertise in the N-CASR space, will be an engine for our pipeline, creating value via multiple drug candidates addressing multiple tumor targets. The backbone of this N-CAT 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 increased by addition of IL-2 variants that induce their proliferation. 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 Cathy Rezzani at the MD Anderson, her pioneering work using adaptive transfer of NK cells has provided proof of concept that NK cells can induce a strong anti-tumor response. That's exactly what we are aiming to replicate with our NK molecules, which are designed to engage efficiently the NK cells of the patients against the tumor. In the middle panel, you can see the detailed mechanism of action of the tetraspecific NK 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-tumor immune response. On the other end, the addition of IL-2 variants, which target the IL-2 receptor beta-gamma complex on NK cells, induce NK cell proliferation within the tumor microenvironment, increasing therefore the number of anti-tumor effector cells. Overall, this platform demonstrates compelling preclinical anti-tumor efficacy, as evidenced by the strong efficacy that you can see on the green graph. Lastly, on the right, you can see our growing pipeline of NK molecules, with Sanofi having licensed two molecules, which I will cover in the next slide. Our most advanced proprietary ENCAT is a tetraspecific molecule targeting CD20 and called IPH6501 for which we plan to file an IND next year. We also have other preclinical targets for which we hope to provide some updates on due course. On slide 13, you can see our most advanced ENCAT program is a CD123 targeted trispecific molecule called IPH6101 or SAR 579 that we have generated in collaboration with Sanofi. It is now licensed to them and currently in phase one trial. We also announced over the summer that Sanofi has selected for further development a second drug candidate. It is IPH6401 or SAR514, which is a BCMA targeted tri-specific ANCET molecule, which is using Sanofi cross-odile molecular formats, which shows the versatility of our platform. We have announced 13 million euros in milestones to date from this partnership. On slide 14, we are pleased to have a few presentations at ASH, highlighting the development for LACUTAMAV, as well as several updates for the Enquete platform. This includes the two programs with our partner, Sanofi, and another presentation from our CSO, Professor Eric Vivier, who will present the Enquete platform, including our latest update published last month in Cell Reports Medicine. We will have also updates at the ESMO-IO conference in December for our anti-CD39 program called IPH5201. I will now turn to Mondaire for a summary of the catalysts and flows. Thank you, Yanis. Please move to slide 15.
spk06: 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 heard from Joyce, in our phase two Telomax study for lacrytamab 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 trials are underway, and we continue to advance the adenosine pathway agents in the clinic, where we look forward to sharing our Phase II plan in due course. In parallel, we continue to develop our NCAT technology platform, including with our partner Sanofi, and we are very encouraged by the preclinical results from our next-generation NCAT cell engagers. 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 dates on our Proprietary Enquete, EPA 65-1, 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 INEE. 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 medicines to patients. We look forward to keeping you updated on our progress. That concludes our prepared remark. We will now open the call to questions.
spk09: At this time, I'd like to remind everyone, in order to ask a question, simply press star, then the number 1 on your telephone keypad. Again, that is star 1. Our first question will come from the line of Yagal Nokomovich with Citigroup. Please go ahead.
spk07: Hi, Mondar and team. Thank you very much for taking the question. I just had two, one on Telemat and then one on the Tetra-specific ANCET. So on Telemat, I was just interested in the cohort three, which I know is the one with the non-expressors. You still had some good responses, albeit not all of them characterized as TRs. I was just curious, is that because those patients are still expressing some low level of the target KAR3DL2, or is there another reason? And then on the tetraspecific ANCET, 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 tetraspecific platform can do above and beyond the known target, as opposed to introducing a totally new variable in addition to the Tetra-specific ANCET. So, if you could just elaborate on your thinking there. Thank you.
spk06: Thank you, Igor, for the two very important questions. Actually, we'll start with the second one, and I'm going to hand over to Yannis to set the context, actually, of the identification and selection of these targets, and then Justin will address your question about the level of activity we have seen with cohort three. You are absolutely correct. It's not nil, it's not zero. We have some activity and we have some hypothesis to explain actually that level of activity. But let's start with the NCATS platform and the CD20 first.
spk05: Yes, hi again, Yanis speaking. Yeah, I think you're right. We selected CD20 in order to limit the number of variables. With this new tetraspecific molecule, we are really progressing to the clinic a brand new mechanism of action, relying on the activation through NKP-N16, as well as the cytokine in the same molecule. So as we are 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 has also the advantage when you look at the expression, as opposed to other potential validated targets, to be quite stable across a different line of treatment, meaning that if you have like a retuximab relapse patient, a lot of them are still expressing the target, which makes really, from our perspective, the ideal candidate for this first proprietary program in the clinic, knowing that we have also others at the preclinical stage with other targets.
spk06: Thank you, Yanis. 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 preclinical antitumor activity that we have published in various tumor models. May I ask maybe to address your question on why we still have responses in cohort 3 despite the fact that the K3DL2 level of expression is below the 1% threshold?
spk03: Yes, so just as a reminder, the cohort three is mycosis fungoides, and cohort two is the expressing mycosis fungoides, UGAL, as you mentioned. Now, you know, there are different factors. One is, of course, the heterogeneity of tumors. Number two is the assay sort 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 TELEMEC study does have an all-commerce cohort also, which will be looking at an FFPE assay. We're keeping in mind that cohort two and cohort three were a frozen-based assay. So these are sort of the reasons why we believe that you're seeing some low-level activity.
spk01: Thank you. Thank you.
spk09: Your next question will come from the line of Edana Gravosh with SVB Securities. Please go ahead.
spk08: Hi. Thank you for the question. Two for me on Telomac and Lacudamab. 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 fluconamab, and if not, how you plan to do that to meet the loose Project Optimus, I don't want to say guidelines, but almost guidelines from FDA. Thank you.
spk06: Thank you, Diana, for two very important questions. I think Joyce is probably the right person to address. First of all, our thinking about the accelerated approval of lacrytamab in cesarean syndrome and, of course, the evolution of the regulatory environment in the U.S. Joyce?
spk03: 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, so at least at this point in time, you know, I want to say what they're considering for accelerated approval. Of course, as we know, 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 Optimist. You know, interestingly, Project Optimist is just dose justification. And, you know, for us, dose justification, we have looked at dose justification and continue to ensure that going forward the dose is correctly justified. You know, so I think, you know, we've been doing this for drug development for years on end. And, you know, I think for lacudimab, 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.
spk01: Can I have a follow-up? Can you remind us?
spk08: Yeah, can you just remind us? Because it happened longer ago. How many doses you explored and sort of how many patients at various doses?
spk03: So we did explore several different doses.
spk01: We explored both intrap- hello? Hello? Did I just get cut off? I can still hear you. Oh, okay, okay.
spk03: I didn't know if I got cut off. So, we did explore several different doses, both intrapatient dosing as well as, you know, patients who received a single dose throughout. So, we do have several different doses with adequate number of patients and the doses at least that we were able to look at some of the PK and PD.
spk01: Thank you.
spk06: But then if you want, we can follow up and maybe send you the the phase one data that was published. As you know, in in New England a couple of years ago where we have the detail in this escalation.
spk01: And Lancet. Yeah, sorry. Yeah, thank you.
spk09: Your next question will come from the line of Isbayam Pakula Ramakhanath with HTW. Please go ahead.
spk04: Thank you. This is RK from . A couple of quick questions. On the Telomac trial, we know that you're going to present some initial data on the Caesarean syndrome at ASH. But what's the expectation, you know, for the final results of this, of the TILAMAX trial itself? And also, for the same drug, can you highlight a little bit about, you know, your work with BCL?
spk01: That would be helpful. Thank you.
spk06: Hi, okay. Let me, thank you. Thank you for the question. 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 lacrytamab in cesarean syndrome. In other words, sort of targeted product profile. And the second question is an update on the PTCL. And once again, actually, Jason is the right person to address both questions.
spk01: Jason, back to you. I'm here, Jason.
spk03: Sorry, I didn't hear the PTCL question, but let me go ahead and address the Cesarean syndrome question first. So, in Cesarean syndrome, just, you know, from the abstract that was published for us, we did have a global—just as a reminder, this was a very heavily pre-treated population. 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, you know, that we would continue to see encouraging data even in the final data set itself. And I'm sorry, what was the PTCL question?
spk06: I'll take the PTCL one. Just to maybe make sure I got it right, RK, you were asking for an update on the PTCL. And as you know, we have two trials in peripheral T-cell lymphoma. a company around phase 1B trial assessing the level of activity and the safety of lacrytamab in monotherapy. And we have a LISA-sponsored trial. LISA is an European cooperative group well-known in Heme that is testing the combination of lacrytamab with chemotherapy, in particular with the combination of Dremox. And we said at a previous call that an interim or preliminary data will be presented in 2023, so next year.
spk01: Thank you. Thanks for taking the questions. Questions on the line.
spk00: If not, I'll go to offline submitted questions.
spk09: No further phone questions at this time.
spk00: Okay. So we have a question here from Olga Smolenskiva at Brian Garnier. Three parts to the question. Firstly, could you give us any favor what we should expect from the phase one data for IPH5201 at ESMO IO? And do you see any read across for IPH5201 from the recent pause of an anti-CD39 program by surface oncology?
spk06: I think it's fair to say that we will wait for the presentation at SMOIU for further details. As you know, we are starting a phase two trial in non-small cell lung cancer. hope to be able to provide further details on this program very soon. We are unable to comment on other companies and their resource allocation and reprioritization, so we'll stick to our program and the data that will be presented at the end of the year.
spk00: Thank you. Second question from Olga. How do you see IPH 6501 fit into the highly competitive landscape of CD20 targeting by specifics?
spk06: Yeah, another important question. I think Igal, I believe, asked a question along the same line. We are fully aware of the, of course, competitive landscape here, but as Yanis 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 clinical data so far, there is really an opportunity here to differentiate APS65 both on safety but on improved efficacy. And I must also say that this is, again, the first proprietary tetraspecific NK molecule entering into the clinic, and the selection of a validated target was a way to mitigate the risk of going after a completely novel platform, which is the tetraspecific. So that was our approach to really mitigate the risk of the novel platform by choosing a well-established and validated target.
spk00: Thank you. And last question from Olga. Should we expect the final data for lacutimab in cesarean syndrome to include a similar highly pre-treated patient population as per the interim update at ASH.
spk06: Again, I think it may be stating the obvious, but you know that patients in this trial needed to have at least two lines of prior therapy and must be post-MOGA. As you may remember, 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 IV-A and stage IV-B, relapsed refractory, two or more prior line of systemic therapy, including Mogamlizumab. 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 ASHE-abstract efficacy, and we look forward to discussing those data further at the ASHE presentation. Final data, as I said earlier, are due in 2023 for both our microdysphongitis and cesarean syndrome cohorts.
spk09: And as a reminder, to ask a question on the phone, simply press star 1 on your telephone keypad. Again, that is star 1.
spk00: Thank you. We have a couple more questions submitted online. So Jingming Chen at Evercall. Similar 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?
spk06: I'm going to hand over back to Joycen to recap our strategy in terms of development and registration for Lakrita MAB in Cesare MF. Joycen?
spk03: Thanks, Amanda. So, you know, 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, you know, the potential to file for SS-First. That also includes the potential to file for both. All during that time, of course, you know, 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 the data itself will drive the decision. So, you know, the strength of the data will drive the decision. Number two is sort of the regulatory landscape as it starts to evolve will have a major influence on how we look at this. And then third is just our ability to, you know, have a partner, look for a partner.
spk01: Thank you, Joyce.
spk00: I have some further questions submitted online. So Eric LeBerrigo at Stifel. Question one, LeCoutimab has delivered consecutively two highly confirming sets of data in MF and SS. Now, many times in the past, you explained the ability of LeCoutimab 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 on PTCL is the future of lacutumab overall?
spk06: 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, of course, the business case in cesarean and also the potential in MF and clearly having a PTCL indication would completely change the perspective of this drug moving from maybe just a few hundred million to blockbuster if PTCL is there. I think at this point in time, we need to validate the signal through the Telomac 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 PTCL data to emerge, at least the preliminary data next year, to assess the various scenarios. But keep in mind that we have two shots, if I may say, at goal. We have a monotherapy a trial which is maybe a high risk, but nevertheless, I think an opportunity to identify a single agent activity in a heavily pre-treated and difficult to treat patient population. And we have also the combination trial with the LISA group, which of course, way to explore the potential of lacutamab in these diseases. And of course, these are not the only options that we are thinking of. There are many other opportunities in second line, but also in front line 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 these assets.
spk00: Thank you. Second question from Eric. In telemark, patients are required to be pre-treated with MOGA. You collected very advanced patients on average with six previous lines of treatment. 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?
spk06: Again, I think it's an important question, and similar to what I said earlier, it's difficult to speculate on how heavily pre-treated are the patients that will be recruited in the next couple of months. MOGA was still in the launching phase and even after launch we know that 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 patients with a very late line of therapy and we didn't see a major a change in the access to Mogamolizumab 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, a heavily pre-treated and a median of six line of therapy. I think what is important is, A, that we have an activity and a meaningful activity in patients who have been exposed to Mogamalizumab. That's, I think, number one. And number two, of course, this is an area of unmet medical need because by design in the post-Moga setting, there is no established standard of care. Of course, the data we generate with Telomac would be of importance and, of course, will be discussed with the health authority when we have them.
spk00: 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?
spk05: Thank you, Eric, for your question. Like I mentioned, the 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 there are also in this type of NHL some CAR T's, but they are rather targeting CD19. So I think that what you're saying is correct. a pretty good 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 ones that are in the phase three and late stage development, like the T cell engagers.
spk06: Thank you, Anis. I think we have no more questions 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 will continue to advance the Acutamab program, move our early-stage R&D activity in the clinic, with our next generation NCAT platform. While for Monalzimab, we look forward to further clinical development in early lung cancer with AstraZeneca underway, which further infers, of course, our strategy of building a sustainable business with a robust R&D engine. With that said, I thank you very much. I wish you a wonderful day. Thank you.
spk09: Ladies and gentlemen, that will conclude today's meeting. We thank you all for joining. You may now
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