Affimed N.V.

Good day, everyone, and welcome to AffiMed's second quarter 2024 earnings and corporate update call. At this time, all participants are on a listen-only mode. To ask a question during the Q&A session, you will need to press star 1-1 on your telephone. You will then hear an automatic message advising your hand is raised. As a reminder, today's conference call is being recorded. I would now like to introduce your host for today's call, Alex Medicatus, Head of Industrial Relations at AffiMed. Please go ahead.

Thank you, Livia. And thank you all for joining us today for our second quarter 2024 update call. Before we begin, I'd like to remind everyone that we issued the relevant press release earlier today, and that can be found on our investor relations section of the website. On our website, you can also find the presentation we will be using today. On the call today, we have members of our management team, including Sean Leland, our new chief executive officer, Andreas Harstrig, our Chief Medical Officer, Wolfgang Fischer, our Chief Operating Officer, Denise Mueller, our Chief Business Officer, and Harry Welton, our Consulting Chief Financial Officer. Our financials today will be presented by our VP of Finance, Michael Wolf. The team will be available for Q&A after the prepared remarks. Before we start, I would like to remind you that today's presentation contains projections and forward-looking statements regarding future events. These statements represent our beliefs and assumptions only as of the date of this call. Except as required by law, we assume no obligation to update these forward-looking statements publicly or to update the reasons why actual results could differ materially from those anticipated in the forward-looking statements, even if new information becomes available in the future. These forward-looking statements are subject to risks and uncertainties, And actual results may differ materially from those expressed or implied in these statements due to various factors, including but not limited to those identified under the section entitled risk factors in our filings with the SEC and those identified under the section entitled forward-looking statements in the press release that we issued today and filed with the SEC. With that, I'll turn the call over to Sean. Sean?

Thank you, Alex, and good morning, everyone. I'm excited to speak with you today as the new CEO of AFIMED. Although I am only a few days into this role, I'm eager to share my initial thoughts with our shareholders and the financial community. My decision to join AFIMED was data-driven. After thoroughly reviewing AFIMED's portfolio of innate cell engagers, I'm impressed with the platform and firmly believe we are on the verge of something transformational. The commercial potential is quite significant as we have achieved clinical proof of concept across three assets, each with distinct indications. This progress is particularly encouraging for the many advanced refractory or relapse patients who have limited options across indications such as non-small cell lung cancer, Hodgkin lymphoma, and acute myeloid leukemia. Importantly, Affymed's diverse clinical portfolio offers valuable strategic options for our business and, from my perspective, is an enviable position in the biotech world. My immediate commitment to you, our shareholders, is to hit the ground running and to secure funding to support our promising clinical programs. I look forward to engaging with our current shareholders and prospective investors alike I will be speaking with those already familiar with the current AFIMED data and new investors to share my enthusiasm over the clinical pipeline poised for numerous data readouts in the next 12 to 24 months. Although the capital markets have been challenging to biotechs in 2024, I am confident our compelling clinical data differentiates us and will allow us to further extend our runway. Additionally, I am energized to thoroughly examine our business development strategy and broaden our relationships with pharma partners. Innovation is at the heart of our industry, and I am particularly interested in exploring how creative partnering approaches can advance our clinical development, broaden our clinical development strategy to reach more patients faster, and expand patient access to our therapies. During the interview process, I was impressed with AppyMed's passionate employees and culture. dedicated to developing life-changing therapies to address underserved patient populations. To both survive and thrive, we must achieve operational efficiency and excellence. While I acknowledge the significant organizational changes AFIMED has undergone over the past year, I am committed to continuous improvement and a growth mindset to ensure we are consistently delivering meaningful value to our key stakeholders. Before I turn the call over to Andreas, I want to express my sincere thanks to him and the role he served as acting CEO over the past several quarters. Now over to you, Andreas.

Thank you, Sean, and I'm really happy to have you on board. And also good morning to everybody who's listening to our call. Let me go through our programs in detail and put the new data in perspective. We are happy to report that we again have made progress in all programs. I will start with our AFM24-102 trial, in which we evaluate the combination of AFM24 plus atezolizumab in patients with non-small cell lung cancer who have failed standard of care options. Both the EGFR wild type and the EGFR mutant non-small cell lung cancer cohorts are almost fully enrolled now. Today, we will share with you early efficacy data for the EGFR mutant cohort. As you know, the treatment sequence for patients with EGFR mutant non-small cell lung cancer starts with the application of an EGFR specific TKI. Most patients today will receive third generation TKIs. While these treatments are highly effective in prolonging time to tumor progression, They are not curative for patients with advanced or metastatic disease, and ultimately almost all patients will progress. Treatment options after failure to EGFR-specific TKIs are limited. Platinum-based chemotherapy is standard, but may in the future be replaced by a combination based on amivantamab and chemotherapy with or without lacertinib. While amirvantamab containing regimens have shown some improvement over chemotherapy alone, they are also not curative and all patients will ultimately experience disease progression. If you look at the NCCN guidelines, there are no established treatment alternatives for EGFR mutant non-small cell lung cancer patients who have failed two lines of treatment. The options given by NCCN are either palliative care or single-agent chemotherapy, which is usually associated with low response rates and the progression-free survival of around four months, or the enrollment into a clinical trial. And it's exactly these patients who currently have no treatment options available that we have enrolled into our study. As shown on slide four, a total of 24 patients have received treatment so far. Seven patients are not available according to RESIST, including four patients who deteriorated rapidly, often within the first week on study. These are, for the most part, patients who had a long interval between the screening evaluation and the actual start of trial medication. And we have to assume that they had rapid tumor progression in the treatment-free interval. One patient did not have a follow-up scan. And two patients are in the first two cycles having no tumor assessment yet. On slide five, you can see the patient characteristics. The median number of previous lines of therapy is three. All patients have been pretreated with EGFR targeting TKIs. And the vast majority, more than three quarters, had also platinum-based combination chemotherapy. Only two patients had been pretreated with checkpoint inhibitors, reflecting the general belief in the medical community that EGFR mutant non-small cell lung cancer is not responsive to checkpoint inhibitors. On slide 6, we show that in the 17 patients that are response-evaluable, we have four patients with an objective response, including one patient with complete response and three patients with partial response. all confirmed by sequential CT scans. And eight patients with stable disease, including patients with reductions in tumor volumes that failed the PR threshold, resulting in an objective response rate of 23.5% and a disease control rate of 70.6%. Importantly, the responses appear to be durable and thus clinically meaningful all four responders were on treatment for at least seven months. Important to note, eight of 17 patients are still on treatment with a median follow-up for the cohort of over seven months. While these data are still early, they indicate, like the data in the EGFR-Y type cohort, which we reported earlier this year, that the combination of AFM24 with a checkpoint inhibitor has activity in treatment refractory non-small cell lung cancer patients and may become a meaningful treatment alternative for patients who failed standard of care therapies. It is worthwhile noting that these data are achieved with a regimen that does not contain any chemotherapy, an important distinction from other treatments as chemotherapy is often difficult to tolerate by these heavily pretreated patients. Let us now move to our CD30 targeting isomolecule AFM13 or Symptomic that we are developing in combination with LONK in our registration-directed LUMINISE 203 study in patients with multi-refractory Hodgkin's lymphoma. As you see from the study diagram on slide 8, the initial part of the study consists of four cohorts that are designed to optimize the doses of asymptomic and allo-NK, respectively. OHOTs 1 and 2 are fully enrolled, and all patients have at least one efficacy readout conducted by an independent response assessment committee. As you see on slide 9, all patients were heavily pretreated, having exhausted all standard treatment options, including combination chemotherapy, brentuximab, and PD-1 targeting checkpoint inhibitors. Fifty percent of the patients had also failed stem cell transplant. Given that there are no treatment alternatives for these patients, shown on slide 10, we observe a response rate of 83.3 percent, which I believe is outstanding. This includes six patients or 50 percent with a complete response and four patients with a partial response. It's important to note that three of the four partial response patients have not completed their full treatment yet and are continuing to receive additional cycles. In this context, it may be important to remember our experience from the MD Anderson trial, where one-third of the complete responses occurred at later cycles. On slide 11, I'm also happy to report that cohorts three and four in which we test a higher dose of LONK product, are almost completely enrolled, with 10 of the planned 12 patients on treatment. Enrollment in cohort 3 and 4 progressed according to the planned enrollment schedule, and there were no dropouts of patients during screening. Furthermore, we have now 10 different sites across the whole USA that have actively treated patients on the study. We plan to disclose data from all four cohorts at an upcoming scientific meeting in Q4 2024. Finally, let's review the updated results of AFM28, RCD123 targeting ICE for the treatment of acute myeloid leukemia as shown on slide 13. In this study, we have escalated dosing through six cohorts up to 300 milligrams flat dose weekly. The treatment is very well tolerated with infusion-related reactions, mainly of low grade being the main side effect. At the two highest dose cohorts of 250 and 300 milligrams, we did not observe any dose-limiting toxicities. And in 12 patients, only three patients had a grade 2 infusion-related reaction, responding in all cases to symptomatic treatment. There were no grade 3 or higher IRRs, one patient experienced a short-lasting, self-limiting cytokine release syndrome of grade 1. Infections are a characteristic manifestation of acute leukemia and were seen in approximately half of patients we treated in the study so far. However, no infection was considered to be treatment related by the investigator. The clinical activity is displayed on slide 14. In dose level five of 250 milligram AFM28, we saw one complete response, 17%, and five stable diseases in heavily pretreated patients. Of note, the patient with a complete response was in remission for more than five months. In dose level six at 300 milligrams AFM28, the number of complete responses has increased compared to the data that we reported in our Q1 earnings call. Now three out of six patients have developed a complete response or a CRI respectively for a complete response rate of 50%, indicating a possible dose-response relationship. In addition, two of three remaining patients at dose level six have shown stable disease. These highly encouraging results have led to our decision to expand cohort six by additional six patients to confirm the monotherapy signal that we have seen in the study so far. We plan to give a further update on this data at an upcoming scientific conference. As we show on slide 15, we believe further development of AFM28 in combination with other AML therapies or with cryopreserved allogeneic NK cells would allow us to address, again, an area of significant unmet medical need. The seven major markets, we see over 14,000 patients per year who fail at least two lines of standard therapy and require a new treatment option. With this, I will close the overview of our clinical programs and hand over to Michael Wolff for a review of the financial data. Michael, please.

Thank you, Andreas. Balance sheet and income statement highlights are shown on slides 17 and 18 of the presentation. A quick reminder that consolidated financial statements have been prepared in accordance with IFRS as issued by the International Accounting Standard Board or IASB. The consolidated financial statements are prepared in euros. Since our financials are described in detail in the press release we issued this morning, I will only provide highlights on this call. We ended the second quarter with cash, cash equivalents and investments of 34.4 million euros compared with 72 million euros on December 31st, 2023. Based on our current operating and budget assumptions, we anticipate that our cash and cash equivalents and investments together with anticipated proceeds from the ATM program and the sale of UpCheck will finance us into the second half of 2025. Net cash used in operating activities for the quarter ended June 30, 2024 was 16.5 million euros compared with 33.3 million euros for the quarter ended June 30, 2023. Total revenue for the quarter ended June 30, 2024 was 0.2 million euros compared with 1.4 million euros for the quarter ended June 30, 2023. R&D expenses for the quarter end of June 30, 2024 were 11.7 million euros compared to 25.3 million euros in 2023. G&A expenses for the quarter end of June 30, 2024 were 4 million euros compared to 6.3 million euros for the quarter end of June 30, 2023. Net loss for the quarter end of June 30, 2024 was 15.5 million euros or one euro and one euro cent per common share, compared with a net loss of 29.4 million euros or one euro and 97 euro cent per common share for the quarter ended June 30, 2023. Now, I turn the call back to Sean for final remarks. Sean?

Thank you, Michael. As you listen to Andreas' update on our clinical programs, I hope you share my enthusiasm about the robustness of our science and data, as well as the potential of our therapies to address significant unmet medical needs. For instance, on AFM24, the data generated to date in both the non-small cell lung cancer EGFR mutant and wild-type cohorts are encouraging and supports our hypothesis that the combination of AFM24 and PD-1 targeting may act synergistically on the immunity cycle. It is remarkable that this can be achieved with a chemotherapy-free approach, and we look forward to sharing additional data this year from the non-small cell lung cancer EGFR wild type cohort in Q4 of 2024. For our ASCIN2MIG program, the patients enrolled in the Luminize 203 study are critically ill with advanced disease and no remaining approved treatment options. our impressive overall response rate of 83% is a strong indicator of the promise of our approach. And when considered in the context of approved products, our data is very compelling and a much more heavily pretreated patient population. I look forward to sharing additional results from the study soon as we near completion of enrollment in cohorts three and four in Q4 of 2024. We are encouraged by the AFM28 monotherapy There is a clear and strong signal, which is the basis for the expansion of dose cohort six by adding another six patients. We continue to believe there is potential for higher response rates and perhaps greater durability in a combination development approach. Relapsed refractory AML is a difficult disease to treat, and there is much room for improving response rates, given what's seen with currently approved therapies. with CR-CRI rates in the range of 15 to 30 percent. While we need more data and durability, the data we are seeing here underpins my enthusiasm for this program. Before we open the call to questions, I would like to express my sincere gratitude to both the Management Board and Supervisory Board for entrusting me with this important role. Lastly, I want to reaffirm my commitment to you, our shareholders. I'm dedicated to increasing shareholder value through the successful execution of our clinical development programs, achieving milestones, forging new partnerships, and advancing our transformative therapies closer to patients who need them most. With this, I thank you all for your attention, and we are happy to take any questions that you may have. Operator?

Thank you. Ladies and gentlemen, to ask a question, you will need to press star 1-1 on your telephone and wait for your name to be announced. To withdraw your question, simply press star one one again. Please stand by while we compile the Q&A roster. Now, first question coming from the line of Mari Raycroft with Jefferies. Your line is open.

Hi, good morning. I'll say welcome to you, Sean, and congrats on the progress and thanks for taking my questions. I'll start with one quick one on AFM24. For the new EGFR mutant data, just wondering if you're observing any differences among patients who had prior third-gen TKIs versus those who are getting first or second-gen TKIs.

Hey, Mari. Sean, thanks for the question. Andreas, do you want to respond to Mari's question?

Yeah. So, good question, Mari. No, we have not seen any differences. In fact, when we look at our four responders, three of the four responders have been pretreated with third-generation TKI. So there is obviously no cross-resistance or no lower response rate if a patient had had third-generation TKI compared to a first- or second-generation TKI.

Got it. Okay, that's helpful. And then for the aluminized study, I'm just wondering if you can remind me what expectations are for the higher N-Casol dose for cohorts three and four, and are you seeing any biological efficacy or safety differences between the 200 and 300-meg doses for cohorts one and two?

Yeah. Thanks, Mark. Andreas, do you want to respond to this question as well?

Yeah. So for the asymptomic dose 200 and 300 milligram dose, So far, we have not seen any differences in terms of response rate. So this is equal across the two cohorts. In terms of the cohort three and four, as a reminder, we do use a higher cell dose here. This is a cohort that is currently in evaluation and enrollment. The early data that we see are very encouraging, but I think we just have to wait until the data across all The 12 patients have matured, which we will be able to disclose in Q4 2024.

Got it. Okay. And when you do the update in the fourth quarter of this year, will you have the go-forward doses selected at that point as well?

Andreas, you want to speak?

Yeah, this would be the aim. If you look at the study protocol, out of the four initial cohorts, we will select two cohorts for continuation in stage one of the Hodgkin lymphoma program. And as the data matures, we believe that we will be able to make a data-driven decision here.

Got it. Okay, thanks for taking my questions. Thanks, Mario.

Thank you. And our next question, coming from the line of Dana Gerspach with Learing Partners, the line is open.

Hi, thank you for the question. Welcome, Sean, to APMED. I wonder, as you step back and look across these three programs, if you, a question to Sean and to Andreas, how you're considering your development strategy. I think I noticed a change in AFM 28, whereas the last update You know, the plan was to immediately find a partner to combine with NK cells, and now I heard something that was a little bit more ambiguous, more broadly thinking about combination partners. So if you could comment on AFM28 and also whether you're considering different approaches for AFM24 as you move forward. Thank you.

Yeah. So, Dana, thanks for the question as well as the welcome. Maybe I'll start and then turn it over to Andreas. as it relates to AFM 28, I mean, if you, you know, think back to the last update we provided, right, you know, we didn't have the data that we have in hand today. I mean, I think seeing the encouraging monotherapy activity with, you know, three out of six patients, you know, showing a CR or CRI is quite encouraging. I mean, I think it's important to note that in this you know, relapsed refractory setting. And keep in mind, most of these patients have seen, you know, three or more prior lines of therapy, you know, to see a 50%, you know, CR, CRI rate, you know, as we are, you know, continuing on in dose escalation is quite encouraging when, you know, comparable therapies are typically showing a CR, CRI rate, you know, in the 15 to 30% range. So, I mean, I think, you know, we're starting to see kind of this potential dose-response relationship, which, you know, I think leaves us a bit more encouraged, you know, with the monotherapy activity. I think, as we've seen with the, you know, asymptomics program, you know, we do think that there is additivity or synergy that exists in particular with allo-NK cells. So, I mean, you know, under that context, you know, if we add allo-NK cell to AFM28, could we see deeper and more durable responses? I think there's the potential for that. But I think, first and foremost, we're highly encouraged by the monotherapy signal. And by adding these additional six patients, we'll be able to get a stronger sense of how encouraging that monotherapy signal is. But I'll pause here and see if Andreas has anything to add.

I think you covered AFN28 very well. Again, these are, as always in clinical development, data-driven decision, and I just want to emphasize, if somebody had told me when we started AFN28 that we will have a 50% complete response rate, I would have said, yeah, great, I take it. But these are just outstanding data, and I think we have the obligation to find the best way to bring this treatment to patients. This can be in combination with either standard of care drugs that are used in AML. It can be in combination with an NK cell product. So there are clearly multiple options. And yeah, AFM28 has become for us a very interesting, a very promising product. The same is true for AFM24. Again, non-small cell lung cancer, a very challenging disease. especially if patients are pretreated with at least two lines of therapy. Again, this is the case for both of the cohorts, EGFR white type, EGFR mutant. You don't have any standard of care treatments. And to see a consistent efficacy result, and I think this is the most important thing, that's not just one number that pops up, but you see consistency, you see objective responses in both cohorts, you see durable responses in both cohorts, Again, something that we believe is highly encouraging can really change the life of patients in need. And we will have to find the best way as an organization to move these programs forward to bring them to patients. Whether this will be best done in a partnership or to a certain extent initially alone as an AFIMED organization, we will have to evaluate all strategic options and But the most important thing is that we have data to build on. And that's where we are right now. And I just can't share my enthusiasm about this data. It looks really, really very promising.

Maybe one follow up on AML. Is there a durability of response threshold you guys would like to see to think about a potential single agent path forward?

Yeah, it's a good question. Andreas, do you want to respond to Dana?

Yeah, I mean, responses, of course, have to be durable to be meaningful for our patients. In these heavily pre-treated patients, any single agent that produces responses or progression-free survival that is in the range of six months I think is meaningful, especially if this can be achieved with very low toxicity. And so this would be, I think, a threshold for a single agent development. But again, given the very good side effect profile and the very unique mechanism of action, I think we also have any multiple kinds of options for combination development, either with standard of care drugs or, as we mentioned already, with allogeneic NK cells.

Thank you.

And our next question coming from the line of Bill Jahangir with Choice Securities. Your line is open.

Hi, congrats on the progress and welcome, Sean. I'm on to Pripa. I had a follow-up question on AML. I was wondering if you guys could maybe give us a hint of some of the mutations that some of these AML patients harbor because I know the response rates are different in different subsets and Regardless, your data is very impressive in the monotherapy so far, but any sort of color on that would be great.

Hey, Bill. Thanks for the welcome. Andreas, do you want to respond to Bill's question as it relates to mutations that we've seen thus far on patients treated with AFM28?

Yeah, so we are currently combining and collecting all this data What we see so far, it's a mixture, so we do not have unusual selection. I think it's probably quite representative for the mutation pattern that you see in a pretreated AML population. And we will have all this data ready for our upcoming data release at a scientific conference in Q4. Thank you.

Thank you.

And our next question coming from the lineup. Lee, what's up with cancer? Your line is open.

Hey, guys. Thanks for taking our questions. And Sean wants to add my congrats as well. So I guess for ASM13 cohort one and two, wondering if you can comment on, I guess, how many of these 12 patients is still on study? And what are you seeing in terms of durability? And then also curious for the patients that achieve partial response, wondering if you can comment on the kinetics of the response and trends you're seeing in terms of deepening response.

Haley, thanks for the welcome and congrats. Andreas, do you want to follow up on her questions?

Yeah. I think for duration of response or general duration questions, the follow-up is just too short. You know, we initially had a staggered enrollment. Obviously, the two patients with progressive disease who did not respond have left the study, but the majority of patients is still on treatment. As we said, for example, three of the four patients with a PR are still on treatment. The complete responses that we have reported, the six complete responses, they were all complete response after the first cycle. So there is obviously technically no way to see a further kinetics. But when we refer or when we take into account our experience that we had at MD Anderson, roughly one-third of the patients that ultimately achieved a complete response were partial responders after cycle one and then with additional cycles got into a complete response. So we will have to wait until we have completed the treatment of these three additional patients to be able to really comment on the response kinetics. Again, the six patients that we are reporting right now as complete response all were complete responders after the first cycle.

Okay, great. And I have a follow-up question in terms of the screening failure rate. I wonder if we can just comment on what you're seeing now. It seems like you made pretty nice enrollment progress for Cohort 7-4. Was that more driven by maybe more size or initial data or maybe a combination of factors? And is this sort of a good run rate of enrollment pace that we should be thinking about as you're moving to the randomized portion?

Yeah, we are really happy with enrollment in cohort three and four. But this is something that you often see in trials, that initially you have to do some training of the sites. And then we also had a couple of patients who just dropped out because of infectious complications. Now I think sites have the right feeling for the right patients. We also have more sites. I'm very encouraged by the enrollment. You know, whenever you move from a single site study, especially if it's an academic center like MD Anderson, there are always some concerns whether you can reproduce this in the real world setting, if you will. But now with 10 sites actively enrolling patients and still producing these outstanding data, I think it's indicating that this is a treatment that can really be given across the country and can reach many patients in need. are because basically every site that has some experience with lymphoma treatment can administer this type of treatment.

Thank you.

And our next question, coming from the line of Yonan Zuz with Wells Fargo Securities. Yonan, it's open.

Hi. Thanks for taking our question, and congrats, Sean. And this is for Yanan. So my question is on asymptomic. You mentioned that the response rate is consistent across cohorts one and two. I wonder if there is a dose response on the CR rate. Thank you.

Thanks for the welcome and congrats. Andreas, do you want to speak to the potential dose response with asymptomic?

Yeah, as we already said, currently we have not seen a difference in responses between quads 1 and 2, so no difference in 200 or 300 milligrams of the symptom. We also have not seen any difference in toxicity. Again, with longer follow-up, we will have to evaluate whether there is a difference in terms of duration of responses. Now with quads 3 and 4, we ask the second important question, which is, was there a higher dose of the LNK cell will make a difference, but here we have to wait until the data is a little bit mature. But again, in terms of response rates, no difference between 200 and 300 milligrams.

Got it. And that includes the CR rate, right?

Yeah.

Okay, great. Thank you. And AFM24, can you remind us the bar on AFM24? PFS and any updated data on PFS you can share with us on both WildTie and Mutant. Thank you.

Yeah. Andreas, do you want to speak to that question?

Yeah. So, again, for the wild type, we have the data that we disclosed at our last earnings call where the PFS was 5.9 months. We have not an updated PFS for the additionally enrolled patients. This is something that probably will be available Q1 2025. We will have response data for the expanded EGFR white type cohort in Q4 of this year. As we reported for the EGFR mutant cohort today, we still have roughly 50% of the patients that are response-evaluable on treatment with a meaningful up of seven months. So we don't have the mature PFS yet. Again, these responses that we see, and this is exactly the same with EGFR-Y type and the EGFR mutant cohorts, they seem to be durable. As we said, all four responders have been on treatment for at least seven months. When we reported EGFR white type cohort, again, the responses were lasting seven, eight, and nine months. And still, some of these patients were ongoing at eight and nine months. But we need for both cohorts a little bit more maturation of the data to have a final PFS number. As a reference, again, single agent chemotherapy, or even chemotherapy in combination with an VEGF inhibiting agent like Siremsa usually produces PFS data of four or 4.5 months. So seeing roughly half of the patients still on trial at seven months is for us highly encouraging as the data in the UGFR-Y type cohort where we have close to six months of PFS.

Got it. That's super helpful. Thank you.

Thank you.

And our next question coming from the line of Brad Canino with Stiefel. Your line is open.

Hi, and thank you. Sean, nice to hear you on the call. I do have a question for you. I think when I look at your past history, a majority of your experience has been the development of drugs with distinct monotherapy activity and I think here you've got AFM24, the activity signal derived from single arm data uncontrolled in combination with a drug that is known to have some limited salvage activity. So it would be great if you can walk me through your diligence process and how you vetted the potential contribution of the parts or perhaps the right word is synergy from AFM24.

Yeah. Thanks, Brad, and great to hear from you. I mean, I think, you know, overall, you know, looking across kind of the The portfolio of AFIMED products, I mean, I think what's quite encouraging is the fact that there's great validation of the platform technology across not only solid tumors in terms of what we've seen with AFM24 in combination with anti-PD-1, but also in the hematologic malignancy space as it relates to what we've seen with Asymptomeg, and then also with what we've recently been seeing with with AFM28. I mean, I think that there is clear signs that there's monotherapy activity that's been seen with these products, but I also believe that there is perhaps greater potential with the combinations. So that is really kind of what was seen in my due diligence. I think a lot of my due diligence was also looking at where this data stacks up against competitors, Brad. And, I mean, kind of taking them kind of like one step at a time here, right? I mean, you look at the SymptomIG program, you know, seeing a 83%, you know, response rate with a 50% CR rate. And what is arguably a much more heavily pretreated population than what's in, you know, the Edcetris label, for example, and then also what's in either the Opdivo or Nivolumab labels, I mean, this is highly encouraging. I mean, this is something that, you know, from my perspective could be a best option for patients with Hodgkin's lymphoma. And I mean, this is a very heavily pretreated patient population. So, you know, I also look at this from the perspective of, you know, being able to address unmet medical needs. And yes, historically, I've focused in kind of the precision oncology monotherapy space. But You know, I think more and more as we see the field of oncology move, you know, a lot of that movement is towards that of combinations. I mean, I think with AFM24, I mean, I think as Andreas has highlighted, there's not really any great options for these patients in the settings where we are studying them. I mean, typically... you do not see, you know, for the EGFR mutated cohort, you know, which is what we kind of focused on as it relates to the update today, you know, I mean, there's not really anything out there, you know, for those patients. I mean, you're basically talking in a single agent, you know, chemotherapy or going on to a clinical trial, which is kind of the NCCN recommendations, you know, post EGFR TKI and you know, post products like amivatinib and lazertinib. So, I mean, I think that the data is highly encouraging, and it's also quite encouraging, you know, since we typically don't see any monotherapy activity of anti-PD-1 in this population, this idea of, you know, being able to combine, you know, two therapies, one that targets, you know, the innate immune system and one that targets the adaptive immune system, you know, there seems to be a synergistic effect and, you know, there seems to be a really nice benefit in these patients who really have no other therapeutic options.

I appreciate all the commentary around that. Thank you.

Thank you. And our next question coming from Delana. So I am Pekula Ramakhan with AC Wainwright. Your line is open.

Thank you. This is Sarkia from AC Wainwright. Welcome aboard, Sean. Most of my questions have been answered. I just have a quick question on the AFM24 program. Now that we have data from both the wild type and the mutant EGFR patient cohorts, how do you plan to take these studies forward? And is there a plan to expand these cohorts initially? to strengthen the data before going into the next level of clinical development. That's it from me.

Thanks. Thanks for the question and as well as for the welcome. Andreas, do you want to speak to his question?

Yeah, so I think these decisions are a very good question, or will be data-driven. What we have done, especially for the EGR-Y type, we have already expanded. As you know, we initially reported 17 patients. We have now a cohort that is basically fully enrolled with a target patient population of 40 available patients. So this will give us a significantly broader data set. Again, we expect to have response data by year-end and then PFS data early 2025, and then we will have to make strategic decisions how to proceed. Again, with the PFS that we are currently seeing, also with the tail, with the duration of the responses, we believe that we could beat the standard of care in this area, which would be docetaxel plus minus remesirumab. EGFR mutant is even a more, I would say, deserted field once patients do not respond anymore to TTIs and platinum-based chemotherapy, even palliative care is considered. So based on the data and then if the data mature a little bit more, we will have all these discussions. We also start interactions with the regulatory agencies and then really form out the best way to potential market approval.

Thanks, Andreas. Thank you very much for taking the question.

Thank you. And I'm showing no further questions in the queue at this time. And ladies and gentlemen, that's the conference for today. Thank you all for participating. And you may now disconnect.