Good day, and thank you for standing by. Welcome to Affimed Financial Community Call to discuss data from the poster of the AFM24-102 study and an initial presentation on the data from the EGFR mutant cohort of the company's non-small cell lung cancer study. At this time, all participants are on a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you will need to press star one one on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be advised that today's conference is being recorded. I would now like to hand the conference over to your first speaker, Alexander Fudukidis, Director of Investor Relations. Please go ahead. Thank you very much. Good day, everyone, and welcome to our call today to review data from the AFM24 study for the non-small cell lung cancer EGFR wild-type patients from our poster today at ASCO. As was just introduced to you, we will also present initial findings from our treatment of patients in the non-small cell lung cancer EGFR mutant cohort. As a reminder, today's call is being recorded, and the recording will be made available on our website later today. Before we begin, I'd like to remind you that we also issued a press release, which may be found on the new section of our website. On our site, you will also find the presentation, which we'll be sharing with you today. For our call today, we have Dr. Andreas Harstrick, our Chief Medical Officer and Acting Chief Executive Officer from our management team, and one of our leading investigators for the AFM24 study, Dr. Kim, Professor at Yonsei Cancer Center, Division of Medical Oncology, Department of Internal Medicine at Yonsei University College of Medicine in Seoul, South Korea. Before we start, I'd 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 event. 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 the statements we will be making today, including, but not limited to, those identified under the section 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 Andreas and Dr. Kim to present the data. Yeah. Thank you very much, Alex, and, also, welcome from my side and thank you for listening in to our presentation of the data of AFM24 in combination with atezolizumab in patients with non-small cell lung cancer. Just as a reminder and a summary where we stand as a company, currently, we believe we are one of the clinically most advanced companies looking at, the innate immune system. Alex, we have the wrong slide here. With more than 450 patients, on study across our three clinical programs. Consistently, we have demonstrated a clinical efficacy as monotherapy in multiple, indications. We also have seen compelling efficacy data in combination with both NK cells and checkpoint inhibitors associated with a well-managed safety profile as a monotherapy and in combination. We remain, we maintain, IP, a strong IP position, targeting CD16A on NK cells and macrophages, and we have full global rights for all of our clinical assets. Now, on the right side, you see the rationale why we are combining our ICEs with checkpoint inhibitors. We have seen in our preclinical as well as in our early clinical studies, that treatment with an ICE, namely AFM24, not only induces and activates the innate immune system, exemplified by increased infiltration of natural killer cells into tumors as shown by biopsies. But we have also seen consistently and in a dose-dependent manner, an upregulation of T cell activation markers, upregulation of circulating CD8 cells, as well as an increased infiltration into the tumor tissue. This provides the basis for the combination of AFM24 and PD-1 targeting agents. On the next slide, also just as a reminder, it's important to remember that the mechanism of action of AFM24 is fundamentally different from the mechanism of action of currently available EGFR targeting agents, whether these are antibodies like cetuximab or panitumumab, or small molecule TKI inhibitors like gefitinib or osimertinib. All these currently available EGFR targeting agents, mainly or exclusively work by the disruption of the EGFR signaling cascade, which transports growth and survival signals all the way from the membrane to the nucleus. The limitations of this mechanism of actions are multiple. First, as you see, there are several intermediate pathway steps, and resistance-conferring mutations can basically happen on every level. Most notably and most well characterized, the activating KRAS mutations, which confer 100% resistance to EGFR targeting conventional antibodies. Also, normal tissue uses a signaling pathway for survival, and the disruption of this pathway leads to the well-characterized side effects like skin toxicity or mucosal toxicity. And finally, in order to address a tumor cell by disrupting the signaling cascade, this tumor cell needs to be dependent or addicted to this pathway, and we have learned that a number of different tumors can use alternative pathways to escape EGFR inhibition. Now, in AFM24, we selected an EGFR binding moiety that has a thousandfold less potency to inhibit EGFR receptor phosphorylation, and therefore, AFM24 does not impact the signaling cascade. The only function of the EGFR receptor in the context of AFM24 is to serve as a kind of mailbox address, but the whole killing of the tumor cells is mediated by effector cells, like natural killer cells and macrophages. As a consequence, we do not see the classical side effects like skin or mucosal toxicity. We are not subject to resistance-conferring mutations in the downstream pathway, and we also can address tumor cells with very low target expression. Here is a high-level summary of our clinical program with AFM24 so far. We conducted our monotherapy study initially to define the right dose and schedule. In the monotherapy, we saw already meaningful clinical activity across multiple indications, including colorectal cancer, renal cell carcinoma, and EGFR mutant non-small cell lung cancer. We established a safe and well-tolerated dose of 480 milligrams as a recommended phase II dose, associated with a well-managed safety profile, where infusion-related reactions that usually are confined to the very first infusion are the only noteworthy side effect. In tumor biopsies, we could also demonstrate that we have a simultaneous activation of the innate as well as the adaptive immune system, which is the rationale for the combination that we used in the AFM24-102 study, where we combined AFM24 with atezolizumab. In this study, we have seen objective responses across all expansion cohorts that were tested. We could show that there are no signs of additive toxicity, and both compounds could be given at their full respective single-agent doses. Given initial efficacy data, our current focus is now on EGFR-expressing non-small cell lung cancer, where the two expansion cohorts that are active right now will recruit 40 patients in the EGFR wild- type and 25 patients in the EGFR mutant cohort. What you will see today are early data, interim data from both cohorts. The EGFR wild- type data were published today at the poster presentation at ASCO. As a reminder, this slide shows a graphics description of the study design. As you can see, our patients start out with one infusion of AFM24 single agent, and then go to the regimen of the combination, where we give AFM24 once weekly and use the biweekly approved schedule of atezolizumab. Patients continue on treatment until disease progression or unacceptable toxicity. Tumor evaluations are done every second cycle, so basically every eight weeks. And with this regimen, we have generated the data that we are able and happy to present today. And with this, I would turn over the call to Professor Kim, who will share with you the data of the AFM24-102 EGFR wild-t ype cohort. In contrast to the data published today, the cutoffs that you will see in this presentation has a later date, therefore, the follow-up period is more mature than that was displayed on the poster. With this, I'm happy to hand over to Dr. Kim. Thank you. So hello, everyone. I am Professor Hye Ryun Kim, the medical oncologist in Yonsei Cancer Center, South Korea. I actively participate in, the enrollment of patient in AFM24-102 study. I'm very pleased to share my experience in this meeting. So today, I'd like to talk about the clinical data and patient care experience. Firstly, I'm talking about the EGFR wild- type, in patient. So this is the treatment paradigm of non-small cell lung cancer patient without, driver mutation, including EGFR and ALK and ROS1 patient in the first-line setting, the immunotherapy combined with, cytotoxic chemotherapy is the standard of care in this patient. The after the failure of the first line, chemo, plus minus EGFR inhibitor should be the option in this patient. However, the unfortunately, after the, second-line failure, actually there are not efficient treatment options in this patient. We can consider palliative care or other cytotoxic chemotherapy, which was not used in prior treatment, or we can consider clinical trial. Surely, there are highly unmet needs in those patients. To move on to the clinical data, the 1 or 2 trial. So far, 17 patients were enrolled in EGFR wild-type expansion cohort. Most patients are ECOG performance status 1. The median number of the prior lines of therapy are 2, but range are 1 to 5. Some of the patients received the 5th line of the treatment, or patient failed 2 prior checkpoint inhibitor. These patients are heavily treated patients. Regarding the adverse event, one patient experienced the serious related TEAE. However, the grade 2 infusion reaction and this patient finally resolved it. One patient is some kind of severe serious related treatment-emergent AE, grade 3 liver toxicity, liver enzyme elevation. Infusion-related reaction three times, but this event occurred in just one patient. The safety profiles are well manageable and toxicity is mild. The majority of patients experienced only mild to moderate treatment-related AE. It is some manageable toxicity in the clinical field. The combination with Atezolizumab, the PD-L1 inhibitor, in line with observed toxicity profile of the individual agent. Dosing for both AFM24 and the PD-L1 inhibitor was given at their respective recommended mono treatment alone. So I'd like to talk about the efficacy in our study. As shown in the waterfall plot, tumor shrinkage is observed in eight patients, almost 50 of 50 of the patients. The 70 patients, 70% patients show the disease control rate, including 4 patients' objective response rate, and 8 patients show the stable disease. Of overall, 15 evaluable patients, 1 patient showed complete remission, and 3 patients showed partial response. I'd like to highlight that of 4 patients with the response, 3 of 4 patients did not achieve an objective response rate on prior checkpoint inhibitor. That means the AFM24 combined with atezolizumab would be efficient treatment strategies in those patients, refractory to prior immunotherapy. Also, AFM24, non-small cell lung cancer, EGFR wild- type expansion cohort, show the compelling efficacy that is competitive with the current, second-line treatment. AFM24 plus atezolizumab induced durable response in heavily, pre-treated EGFR wild- type patients, and 3 or 4 patients ongoing at more than 7 months. This, the response is so amazing in the heavily treated, refractory to prior, the immunotherapy. So as shown in this spider plot, the several patients show a deepening of the response after 10 weeks of AFM24 combined with atezolizumab therapy. It is show the rapidly, the regression of the tumor burden. This is, is on the prominent data in those settings. From now on, I would like to share actual patient cases enrolled in, one or two trial. So this patient is, my patient, and 74-year-old male patient, the diagnosis with lung cancer, with large tumor volume and the right upper lobe metastasis with impending obstruction. And the patient have adrenal metastasis, at the time. So this patient failed to prior immunotherapy and chemotherapy and heavily treated patient. So he received the prior third line of treatment. Then we decided to enroll the AFM24-102 trial, and started the fourth cycle on 9 August last year. Then after the second cycle, this patient showed marked decrease of tumor target region, more than 50%. Also, the patient's symptoms and dyspnea is resolved after the treatment of this drug. The next patient is 66 years old lung cancer adenocarcinoma patient with TP53 mutation. Multiple lung metastasis with adrenal gland metastasis. In the clinical field, p53 alteration patient have a very aggressive cancer characteristics. This patient failed prior multiple lines of treatment, including platinum-based chemotherapy, immunotherapy, and chemotherapy. After the failure of prior third line of treatment, this patient started on 31 May last year. This patient showed partial response after the AFM24 and atezolizumab. So it is very big response in those patients. I'd like to highlight here also that this patient did not objective response in prior treatment in this patient. The last patient is 52 years old, male patient, that our colleague in Barcelona, the lung adenocarcinoma, PD-L1 positive, multiple lymph node, lung metastasis, very a huge tumor volume. This patient also previously received a platinum-based chemotherapy and immunotherapy, and the further to prior treatment. After the treatment of AFM24 and PD-L1 inhibitor in this trial, this patient showed amazing response like this, as shown in this CT scan.The to re cap, the latest, AFM24, combined with atezolizumab in the wild type patient. This combination treatment showed a promising clinical activity, in the heavily treated cohort in patients with EGFR wild-type. Disease control rate is 71%, as much as 71%, and 1 patient show the complete response, and 3 patients show the partial response, and 8 patients with a stable disease. All patients full response were resistant to prior checkpoint inhibitors, supporting the hypothesis that combination of these two drugs may provide an alternative strategy to overcome the resistance, to existing therapy for EGFR-expressing tumors. The safety profile was tolerable and manageable based on our experience. The majority of, AFM24 treatment-related AE were mild to moderate, and the study is ongoing. So far, with the EGFR wild-type expansion cohort currently enrolling up to the total of the patients in the 40 patients. I will stop here, hand over to the Andreas. Yeah, thank you for this presentation of the EGFR wild -type cohort, which I believe shows really a very intriguing and very promising activity profile. I'm happy now to share the initial data that were not part of our ASCO presentation for the second cohort, the patients with non-small cell lung cancer and activating EGFR mutations. I think it's important to note that the biology of these patients is different in a number of aspects from the EGFR wild-t ype patients. These tumors are driven by an overactivation of EGFR signaling pathway, and usually these patients are characterized by a very aggressive behavior and rapid progressions. Now, standard of care is also somewhat different, so all patients will receive a specific tyrosine kinase inhibitors. Currently, osimertinib is by far the most frequently used TKI. Now, once patients do no longer respond to checkpoint inhibitors, the prognosis or the treatment alternatives are really bad and very limited. Standard of care usually is a doublet platinum-based chemotherapy. However, outcome is relatively poor, and progression-free survival seems to be shorter than in the EGFR wild-type patients. The most important difference in the context of the study that we are discussing here is that PD-1 or PD-L1 inhibition, or PD-L1 targeting agents, are not used routinely in these patients. And it is believed that PD-1 has very little to no effect, and these tumors are immunologically very, very difficult to address. Again, once patients have failed TKI and chemotherapy, the treatment options are very, very limited. Single-agent chemotherapy is used occasionally. Many patients will go on to palliative care or only to clinical trials. In the current dataset, we have enrolled 21 patients. As you can see, a median age of 61 years. Characteristics for EGFR mutant non-small cell lung cancer patients, there is dominance of female patients over male and Asian patients over white patients. The median line of previous therapies is 3. As you can see, all patients were resistant to TKIs. Roughly 80% of patients were also resistant to platinum-based chemotherapy. However, reflecting the low activity of checkpoint inhibitors, only 3 patients had received the previous treatment with PD-1 or PD-L1. These patients who had, in general, I would say a higher tumor burden and inferior prognosis compared to the EGFR wild- type cohort, we did see a handful more of side effects. Specifically, we saw some patients with neutropenia or neutropenia in association with fever, which resolved in all patients, but likely reflect the heavy pretreatment and sometimes also a very short interval between previous chemotherapy or radiotherapy and start on the trial. Currently, we have 15 patients, or 13 patients who are evaluable for response and are reflected here in the waterfall plot. As you can see, currently, out of these, 13 patients, we have four patients with an objective response, including one CR and three PR patients, as well as additional six patients with stable disease, of whom some have also meaningful reductions in tumor volume. What we have experienced, and it is better shown on the, I would say, on this slide, swimmer plot in the next, is that some of these patients reflecting the very aggressive nature of this disease, especially when you discontinue treatment with TKIs, have a very early progression. A couple of these patients only received a single infusion before showing either clinical or radiological progression, and therefore, would not be available for the treatment response. Next. This is also reflected in the swimmer plot that currently is immature, as the median follow-up is only 3.5 months. As you see on the bottom, we had a number of very early dropouts, and this will be reflected in a refinement of our inclusion criteria, where we need to make sure that these patients with very, very early progression, probably will not be subject to combination treatment. However, if you look at patients who are on treatment for four weeks or longer, you do see that the majority of patients are still ongoing, including these four patients with objective response. This is also reflected in the spider plot. Again, you can see patients with very meaningful reductions of tumor, and in those patients who had any natural reduction of tumor, whether it qualified for a partial response or a stable disease, just missing the definition of a partial response, the tumor control is still ongoing in all patients. I think it is quite obvious that this opportunity represents a very significant market potential. In the seven major markets, EGFR wild- type, if we are looking at patients who are second-line or beyond, represent a patient population of more than 170,000 patients. Even EGFR mutant patients, which is a rarer disease, still has roughly 37,000 patients that would be addressable by this kind of therapy. In conclusion, we believe that AFM24 in combination with atezolizumab has really shown promising data in both cohorts. More mature data in the non-small cell lung cancer, EGFR wild- type. We have shown meaningful activity in patients who have failed chemotherapy and patients who are refractory and never responded to PD or PD-L1. We believe that it is highly unlikely that these results are driven by PD or PD-L1 alone. All responders, as demonstrated, were documented progression on previous PD and PD-L1. Even if we would consider that these patients would somewhat have been resensitized to atezolizumab, the progression-free survival that you can achieve with single-agent PD-1 in these patients is only 2.8 months, and therefore, significantly inferior to the 5.1 months that we have observed in our study. In the EGFR mutant cohort, again, the combination with AFM24 and atezolizumab showed promising early data, indicating that there may be a synergistic interaction, which can improve efficacy results. As demonstrated, EGFR mutant non-small cell lung cancer is considered an immunologically weak subtype, where single-agent immune checkpoint inhibitor has resulted in very poor results. Next and final slide is, as we published earlier this week, we have submitted the data from the EGFR wild- type cohort, combination twenty-four, AFM24, and atezolizumab to FDA. FDA, after review of this data, has designated Fast Track designation to this combination, reinforcing the potential of AFM24 to address an unmet medical need in this patient population. As said, both cohorts, EGFR wild- type and EGFR mutant cohort, continue to recruit patients, and we will provide further update on this data in second half of 2024.... With this, I thank you for your attention, and would give the call back to the moderator and, open the lines now for questions. Thank you, sir. As a reminder, to ask a question, you will need to press star one one on your telephone. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. I see our first question comes from the line of Maury Raycroft from Jefferies. Please go ahead. Hi, congrats on the data today, and thanks for taking my questions. Maybe to start off, I was gonna ask, for the EGFR mutation patients, can you say anything more about the types of mutations that you treated? And you mentioned in the prepared remarks that KRAS mutations have 100% resistance to EGFR inhibitors. Do you have any KRAS mutant patients in your study, and especially as responders? Yeah, thank you, Maury, for the question. So in terms of EGFR mutations, these are the classical activating EGFR mutations. Again, as you know, they are intracellular, so therefore, they are not interfering with the binding of AFM24, which binds to the outside. Initially, patients usually start out with either exon 19 or exon 20 mutations. Usually in the course of disease, many patients will develop a secondary mutation, and the most frequent one is the T790M. Again, as more than 80% of the patients have received osimertinib, we would believe that T790M was the predominant secondary mutation. Now, in KRAS mutation, we did not specifically look at activating KRAS mutations. We know from our very old data, maybe Professor Kim has also some data, but from our old data, when we looked at large populations of patients with EGFR-expressing non-small cell lung cancer, roughly 20% of patients will have a KRAS mutation. But again, based on our data, we would not expect that this mutation has an impact on the likelihood to respond to AFM24. Okay, understood. So you're still, you could still disclose more about the types of mutations in these patients then, in the future? Yeah, we will disclose more about the type of mutations. We are currently selecting the data. Again, KRAS mutation testing is not standard of care in non-small cell lung cancer. Therefore, we would expect that we may not have a full data set on the KRAS mutation status. Understood. Then I'll ask one more question and hop back in the queue. For the 3 of 4 patients in the wild type population who did not respond on prior checkpoint inhibitor but responded on the AFM24 combo, is there anything unique about these patients that you're further evaluating? I guess, do you know what their EGFR and PD-L1 expression levels were at baseline? For example, the one case study that you showed, where the patient got the anti-TIGIT in the frontline setting, that's unique. So just wondering if there's something unique about these patients. As far as we can tell, there's nothing really unique other than that they had a very poor response to a previous therapy. As Professor Kim has shown, all of these patients basically had three lines of therapy, not responding to PD-1. This one patient that we showed had never an objective response to three lines of therapy. So if you will, they are prognostically very bad patients. We have seen responses, irrespective of histology, so we have seen adenocarcinoma as well as squamous cell carcinoma. As you know, we also have a very, I would say, high hurdle, in a way that we are not preselecting for high EGFR expression and/or high PD-1 or PD-L1 expression. So this is really a representation of an all-comers cohort in non-small cell lung cancer with very bad prognosis. Therefore, we believe that these data are specifically strong, let's say, if you would proactively select for very high PD-1 expressers, you may even have better data. But we are really encouraged that we see this in a completely unselected patient population. Got it. Okay, thanks for taking my questions. Thank you. One moment while we compile our next question. Our next question comes from the line of Kathleen Silverman from Leerink. Please go ahead. Hi. Yeah, someone for Daina Graybosch. Our biggest question is, given the competitive setting in EGFR mutants, trying to understand which paths you might follow down next. You know, for example, one path being the Roche path of bev plus chemo, or the second, like J&J with a TKI plus chemo, or something else. Thank you for the question. Just to be sure, so you're specifically referring to next steps in the EGFR mutant patients? Yes, that's right. Thank you. Okay, so, first, I think, for EGFR mutant, we want to let this data mature a little bit longer. We are expecting to see a progression-free survival in the range of what we have seen with EGFR wild- type. If you get to a progression-free survival of around six months, I think you have a competitive drug in patients who have failed both PD-1 and chemotherapy. And in this situation, I think we would have two options. One option would really be to take this doublet combination and run a phase 3 study against the standard of care, which in these patients, again, may be a single agent docetaxel or any other single agent regimen. Expected progression-free survival for these chemotherapy regimens with in third line is usually four months, so a six-month progression-free survival would very well differentiate. One additional option, again, which we are currently looking at, especially to take care of these early progressers, would be a combination with a TKI, even if this patient has no longer progressed on TKI. We see, and then there's also, I think, some experience, and I talked with Professor Kim just before we hopped on the call. If you have a patient, even if this patient is slowly progressing on TKI, once you take the TKI away, you may see a kind of hyper progression where patients deteriorate very, very fast. So, this would be a second option to really keep a TKI in there and add AFM24 and PD-1, and I believe that would be a very active regimen in the second, third line. Again, you would have to run most likely against the standard chemotherapy regimen. Thank you. Thank you. Our next question comes from the line of Yanan Zhu from Wells Fargo. Please go ahead. Hi, thanks for taking our question. This is Kuan-Hung for Yanan, and congrats on the data. So, just on the EGFR mutant, are you still expecting to report PFS data in the third quarter? And if you, you mentioned that the six months PFS, is that the bar for moving the program forward? Thank you. Yeah, so we are still expecting to report PFS data in third quarter. Again, we have to see, PFS is an interesting endpoint because the later you report the data, the better the data are. So but we will have a snapshot on PFS in third quarter. And again, the six months benchmark, I think is an orientation. If you look at, there are multiple examples, especially from the PD-1 literature, where you have some studies where median PFS was not different at all, but still PD-1 or immune-based therapy produced a positive P value and a positive hazard ratio. So we will also take into account the baseline or the tail of the curve. I think if we end up with 5.9 or 6 months median PFS, and given the fact that we will have a tail of the curve as reflected by the long duration of the responses in the EGFR wild- type, that gives you a pretty high chance to run a successful registration program. Got it. Thank you. And one quick follow-up on the, also on the mutant cohort. I'm curious, on, for those four early discontinuation and three discontinuation due, without scan, were those, simply caused by PD or were some of them, caused by, drug-related AE? Thank you. Yeah, this is just from the dropouts, not evaluable because of the progression. So as you know, and there we presented in this prior slide, and these patients have a very heavily treated patient, and there's some tumor biology is so aggressive. In some cases, have very aggressive characteristics. So these patients, their early progressions, even after the treatment of the drug, this is very short time. So not related with the drug adverse event. Yeah, early progression. Oh, got it. Thanks. As Kim said, we had only early progression, no discontinuation due to side effects. I think we had one patient who had a completely unrelated complication, which was an intracerebral bleeding, but without brain metastasis, so. But all the others were early clinical progression. Got it. Thank you for all the colors. Thank you. One moment for our next question. Our next question comes from the line of Swayampakula Ramakanth from HCW. Please go ahead. Thank you. Thanks for taking my questions. In the data that was presented by Dr. Kim from the wild-type cohort, looking at the safety profile, you know, you talked about 1 patient who had three treatment-related AE, which is higher than grade 3. So, is there anything unique about this patient that had this severe toxicity? And, did any of those AEs get resolved? Yeah, this is a toxicity related with Atezolizumab, as I thought, because under this, the liver enzyme elevation is some expected adverse event related with immune checkpoint inhibitor. So, this patient didn't have any unique characteristic to induce the liver enzyme elevation in this patient. So and we judge this patient is related with atezolizumab, not related with AFM24, in my clinic. Thank you for that. And then in the same patient cohort, what's the longest the patients have seen the combination? As I said, we continue with this treatment until disease progression. So now the longest response is close to 10 months. So this patient is 10 months on the combination right now. Perfect. So the last question from me is, looking at the data in totality, what do you think is helping in overcoming some of the CPI resistance with the combination? You know, I'm just trying to understand how you're able to overcome the resistance with this combination? I think our most likely hypothesis, and is supported also by some of the data that we have generated in our monotherapy studies, that we are restarting, if you will, the immunity cycle. So, you do see by the action of the natural killer cells, destruction of tumor cells and liberation of additional tumor-associated antigens. Now, we are also activating macrophages, which will facilitate the processing and the presentation of these tumor-associated antigens to the T cell system. And we believe that we are simply generating new T cell clones, that then will basically continue to drive in combination with the NK cells, these tumor responses. Okay. Thank you for that. One last question from me. In the mutant population that you saw, the one CR, you know, I, I'm just trying to understand if there is any correlation with the PD-L1 status in any of these patients. And can you talk a little bit about the background and demographics of this patient, the one who experienced the CR? Yeah. Yeah. Can we- The one- The mutant. Yeah. Just the same way we have to... Or maybe we can take it offline and send it. Okay. Yeah. Yeah. One second. It was the patient characteristics of the patient with- Yeah. -complete response. It's the PD-L1 status is unknown for this patient because usually in this population, you test for EGFR and not test for PD-L1. So in this case, in the clinic, they did not test for that. The patient had stage 4 disease with some nodal disease, mainly retropectoral nodes. That helps you out a bit. And as you saw in the lines of treatment, first-line treatment in here was ipilimumab, followed by chemotherapy, and then the last line of treatment was a combination of nivolumab with ipilimumab. It was a female. These mutations are more common in the female population as it is, so it's not unexpected. 67-year-old, very much in the rank for this disease as well. So nothing striking there. All the nodal disease was non-pathological in the CT scan. All the target, all the non-target lesions disappeared completely. They are reported as absent for the investigator. Clinically, what the investigator shared with us is that the patient is doing very well, and she doesn't have any toxicities affecting her daily living or any signs of the disease affecting her reading or her status anymore. The mutation in case you want to know, it's also one of the typical ones. It's exon 21 L858R. That's what it is. And just out of- Thank you. Do you want to introduce yourself to- Oh, yeah, I'm sorry. I'm Dr. Daniela Morales-Espinosa. I am Senior Medical Director at Affimed. For the AFM24. For the AFM24 program. Yeah, that it. Thank you. Thank you. Thank you very much for taking all my questions. Really appreciate your answers. ... Thank you. And I show our next question comes from the line of Dara Aazar from Stifel. Please go ahead. Yes, thank you. Good afternoon, and congrats on the data. This is Dara for Bradley Canino. A few from us. How do these patients compare to those in the literature where checkpoint inhibitor rechallenge has shown salvage responses? And what kind of durability should we expect from checkpoint inhibition alone in the background? And I'll come back for a follow-up. I think it's a difficult question because you really have to dissect the literature. The majority of patients, at least that we are aware of, that do have a response to checkpoint inhibitor rechallenge, either after some waiting period or after some intervening therapy, discontinued their initial PD-1, either due to toxicity or, in the earlier series, also due to protocol-specified maximum duration, where some protocol defined 15 or 18 months as the maximum duration. If you really look at patients who have a documented progression on PD-1, we were able to find a couple of series; there is an occasional response. I think there was 1 response in one series, up to 3 responses in the second series. Consistently, however, if you look at the totality of the data in a patient population that is PD-1 pretreated and then rechallenged, in the one series, I think, published by Dr. Watanabe, the median progression-free survival with PD-1 rechallenge was 1.6 months. In the second series that I'm aware of, the median progression-free survival was 2.7 months. So, you do see occasional responses. These responses usually are short-lasted, and if you look at the overall patient population, our median progression-free survival are either inferior or on par with what is reported for PD-1-naive patients. Again, atezolizumab in PD-1-naive non-small cell lung cancer patients generates a median progression-free survival of 2.8 months. So, totality of the data, if you combine response rate and progression-free survival, we see this data as clearly differentiated and clearly superior to what you would expect in with PD-1 alone. Yeah. Thank you. How are you thinking about pivotal development plan, potentially for a pretreated lung for EGFR wild-t ype? Yep. So I think the unique characteristic is that we are here generating a regimen that is completely chemotherapy-free, which I think is also important, and we have not emphasized this probably enough for these patients. Many of these patients in third, fourth line, will not be able to tolerate aggressive chemotherapy. So our possible ways forward, again, we have also now started with this fast-track approval, which will give us more direct contacts to the... Not fast-track approval, fast-track designation, which will give us more contact to the FDA. One possibility, especially, if we see this tail, which is currently produced by the long responders, would be a phase 3 trial, where you would go directly against the standard of care, which in this case would be docetaxel plus, minus, ramucirumab. Again, this regimen will produce your median progression-free survival of 4.5 months and will not have a survival tail. Here we have 6 months, roughly, and a survival tail, which should result in a positive hazard ratio. One upside potential we are currently considering, is to add ramucirumab to this two-drug combination. We would expect that this would further increase the activity, given the fact that trafficking both of NK cells and of T cells is positively affected by the EGF inhibition. This would be the two possibilities, but going directly into a phase 3 registration program is something that we will have to evaluate in the near future and make a decision on. A very last one. For EGFR mutant, standard chemo, are you thinking docetaxel as the standard chemo or platinum-based chemo? How are you thinking about that, or are you open to either one based on how the data ends up evolving? Thank you so much. I don't think that we will use platinum-based therapy in third line. First of all, by definition, in the EGFR wild-type cohort, all patients are platinum refractory. This was a precondition for the- Apologies. I meant EGFR mutant. Yeah, for the EGFR mutant, 80% of these patients are platinum refractory, so this is not a real option for these patients. Again, standard of care would either be docetaxel in the U.S., probably the most frequently used regimen. Internationally, in Europe, people may use gemcitabine as an option. So this would probably be the two, two standard of care drugs that would be available and would also be used in these patients. Awesome. Thank you. Thank you. Once again, if you have any questions at this time, please press star one one on your telephone. I'm showing no further questions in the queue at this time. I'd like to turn the call back over to management for closing remarks. Thank you very much, everyone, for participating. As mentioned earlier on the call, a webcast of a recording of the webcast or the conference call will be available on our website in about 2 hours. If you have any additional questions, please reach out to me, Alex Fudukidis, at 917-436-8102, or send me an email. Thank you very much, everyone, and have a good evening. Bye-bye now. Thank you. This concludes today's conference call. Thank you for participating. You may now disconnect.