Thank you, Jonathan, and thank you all for joining us today for our Third Quarter 2021 results and operational update call. Before we begin, I'd like to remind everyone that we issued the relevant press release earlier today and that it can be found on the investor relations section of our website. On the call today, we have the following members of our management team, Doctors Adi Hoess, our Chief Executive Officer, Andreas Harstrick, our Chief Medical Officer, Arndt Schottelius, our Chief Scientific Officer, Wolfgang Fischer, our Chief Operating Officer, Ms. Denise Mueller, our Chief Business Officer, and Angus Smith, our Chief Financial Officer. The whole team will be available for the Q&A session. Before we start, I will quickly go through the safe harbor statement. Today's discussion 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 statement, 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 Adi. Adi? Yeah. Thank you, Alex, and good morning, everyone. Thanks, indeed, for joining our third quarter update call, and I'm very pleased with the continued progress towards our goal of bringing new and innovative life-saving medications to cancer patients who need them. Our pipeline positions us for several potential value-creating milestones through the end of 2022. Today, in addition to providing an update on our leading programs, we will spend a little bit of time to introduce you to AFM28, our most advanced preclinical innate cell engager, which is expected to enter the clinic in 2022. On slide three of the presentation that we made available to accompany our call today, we summarize Affimed strategy for developing our innate cell engager. We introduced our three-pronged development strategy to you about a year ago. As we said to you then, we believe the strategy allows us to explore different development approaches, thereby increasing the probability of success for each of our molecules. What we have learned to date about the safety of our molecules is indeed supporting not just monotherapy, but also combination approaches. The first approach, where the patient's own innate immune system is still functional, indeed involves developing our innate cell engager molecules as a monotherapy. Our combination therapy approach involves pursuing novel therapeutic combinations, including combinations with NK cell therapy and other I-O to I-O therapies such as checkpoint inhibitors. In the case of NK cell combinations, the combined cells create CAR-like NK therapeutics that seek out and destroy tumors. An example of that is our investigator-sponsored clinical trial at MD Anderson Cancer Center. On slide four, we are showing where we are with our leading innate cell engager, AFM13 and AFM24, and the recently added AFM28 in a nutshell. All three of these innate cell engagers bind to CD16A on natural killer cells and macrophages with high affinity and also bind to specific targets on cancer cells to bring the innate immune system to fight against cancer. This slide shows our AFM13 innate cell engager targets CD30-positive lymphoma, AFM24, EGFR-expressing solid tumor, and AFM28, our newest candidate, CD123-positive AML indications. We are embarking on a broad development strategy for each of our molecules, which we believe will be the basis for continuous data flow from our pipeline over the next several quarters. Since we introduced you to our three-pronged strategy, we've also made a lot of progress to support our claims. We have published clinical and pre-clinical data that make us quite confident about the path that we have set for our company. Our goal in all of these efforts at Affimed is to bring innovative therapies to cancer patients who are often out of these options when it comes to managing their disease. These are very sick patients who frequently see their disease return after multiple lines of treatment. Very proud to have been able to offer these underserved and frequently without hope patients another opportunity to fight their disease. As we have shown, for example, with AFM13, and in particular in combination with natural killer cells. With that introduction, let me give you a quick update on our program. Jumping now to slide six. This shows a snapshot of where we are with AFM13. Our registration-directed study of AFM13 monotherapy in relapsed refractory peripheral T-cell lymphoma is on track to complete enrollment in the first half of 2022, and we expect to provide guidance about timing for data as we get closer to the completion of enrollment. We're also very pleased to share with you that the investigator-sponsored clinical trial at MD Anderson Cancer Center evaluating cord blood-derived natural killer cells pre-complexed with AFM13 is going very well. As of October 31, a total of 18 patients have now been enrolled in this study, including 12 patients at the highest dose, where we use 10 to the 8 NK cells per kg patient body weight. We can confirm that no dose-limiting toxicities have been observed, and we continue to be encouraged by the response rate. To date, our key learnings are that the dosing regime is well-tolerated and can drive robust antitumor responses in heavily pretreated patients. Our goal is to continue to gather robust data on safety and efficacy, and accordingly, the MD Anderson have submitted a protocol amendment to allow for an expansion of the study to treat up to 40 patients at the highest dose, now including Hodgkin lymphoma patients and CD30-positive non-Hodgkin lymphoma patients. Finally, we plan to present updated data from this study at a company-sponsored event in mid December and expect to provide additional details on the date and time for this event in the coming weeks. We're also very excited about our progress with AFM24, where we believe the execution of our three-pronged strategy will allow for a continuous data flow of data over the course of the next several quarters. Andreas, our Chief Medical Officer, will now tell you more about where we are with AFM24. Andreas? Yes. Thank you, Adi, and good morning, good afternoon to all of you. It's my pleasure and my privilege to give you an overview of our development program with AFM24 and to review some of the recent progresses that we have made in this program. If we move to slide eight, this slide gives you an outline of the development strategy for AFM24. As you'll see, it is a very comprehensive, very broad development approach. We expect to investigate AFM24 as a monotherapy and in combinations with either our PD-L1 inhibitor, atezolizumab, or with autologous NK cells in a total of seven different indications across nine expansion cohorts. This broad approach is intended to deliver the highest probability of success for AFM24, both as single agent and as combination partner. On slide nine, we demonstrate the process that we used to select indications and to maximize a probability of success. The selection of the indications for each studies was based on a very thorough and very comprehensive analysis that used the data of more than 10,000 patients across 144 tumor subtypes. These were initially ranked based on 20 criteria that included, but are not limited to, factors like EGF receptor expression, involvement and function of the innate immune system in the tumor microenvironment, but also looking at unmet medical need and potential paths to market. If we can move to slide 10, we show you the general concept that applies to all of our studies. All studies are based, as I said, on a selection of indications that, in the individual situation, we believe have the best chance of therapeutic success. The individual cohorts in each of these studies follow an optimized Simon two-stage design. This design provides us with an opportunity to make gated investment decisions. In the first step, each cohort will recruit 12-18 patients after which we have a pre-planned interim analysis. This interim analysis is associated with predefined success thresholds. In the case that the individual success thresholds are met, we will recruit up to 40 patients in each cohort, and we believe that this number of patients will give us solid data to start conversations with regulatory agencies about registration strategies. Furthermore, since these are open label studies, we will have the opportunity for interim data readouts. With that said, let me update you on the development of AFM24 in our monotherapy study, which is shown on slide 11. As you are all aware, the initial part is a dose escalation part in order to define the recommended phase II dose. It is important to reiterate that the goal of the dose escalation part was to identify the pharmacologically active and safe dose of AFM24 as fast as possible. Therefore, in the dose escalation part, there was no selection of patients with tumors that are more likely to respond to single agent as defined by our indication selection process. Slide 12 shows you the recruitment status so far. Up to now, we have recruited 29 patients across six dose cohorts. As you can see, the study population covers a wide range of tumor indications, with colorectal cancer harboring either RAS or RAF mutations being the most frequent tumor type. Also important to note that all these patients were heavily pretreated with a median number of previous therapies of four and a range of two to eight previous therapies. All patients had exhausted all available treatment options for their given tumors. On slide 13, we provide a summary of the patients that were treated at the 480 mg cohort. Of note, four out of six patients are still receiving therapy with AFM24 as they are deriving clinical benefit according to the assessment of the treating physicians. Two patients have shown stable disease beyond three months and continue treatment. Of specific note, patient five, while classified with progressive disease, has experienced a meaningful clinical benefit and also continues on treatment. We plan to submit detailed data from the dose escalation for a presentation at a medical conference in the first half of 2022. Moving on, we are pleased to announce that we have determined that 480 mg is a safe and pharmacodynamically active dose, and will be our recommended phase II dose for weekly administration. As outlined in slide 14, this decision is based on a comprehensive review of safety, pharmacokinetic, exposure, and pharmacodynamic data, including CD16A receptor occupancy on peripheral and NK cells. As supportive pharmacodynamic data, we have also measured the panel of serum cytokines and markers of immune cell activation, which exhibit continuous activation of NK cells at doses of greater than 160 mg. From a safety perspective, no dose-limiting toxicities were observed at either 320 mg or 480 mg. In the next two slides, we share the data on the pharmacokinetics and the receptor occupancy that has supported the recommended phase II dose decision. On slide 15, you'll see the PK profiles of all dose cohorts. As shown on the left side, we observe a proportionality of dose and exposure at doses of 320 mg and 480 mg, which indicates that we achieve saturation of target-mediated elimination by EGFR. Meaning that EGFR receptors at these doses are likely saturated. In the graph of the right side, you also see that the trough levels that we are reaching with 320 mg and 480 mg, shown in green and blue dots, are comparable to the cetuximab trough levels at the marketed cetuximab dose, indicated as a gray shaded area. If you move to slide 16, we review here the data that we have obtained with CD16 receptor occupancy, and I will take a minute to walk you through the slide. On the left graph, you see the measured CD16A receptor occupancy on circulating NK cells. As you can see that we initially see an increase in CD16A occupancy with increasing doses, which plateaus at 480 mg, indicating a saturation of CD16A in the periphery. Now, the important question is how does this translate into the tumor, and how is this correlated to activity? On the right, you see two curves from our in vitro studies. The blue curve is tumor cell killing by NK cells in the presence of AFM24. The red curve is CD16A receptor occupation. As you can see, maximum tumor cell killing is achieved as dose ranges that are associated with relatively modest CD16A occupancy. It is important to note, though, that when we speak about relative receptor binding, let's say of 10%, this does not mean that we have only activated 10% of NK cells. Every NK cell has bound AFM24, but on the individual cell level, there is a 10% occupation of available receptors, which already translates into maximum cytotoxicity. Now, the vertical line here indicates a drug level of AFM24 we expect in the tumor at a dose of 480 mg. For this calculation, we have taken a very conservative assumption, which is that AFM24 concentrations in tumor tissue will be 200-fold lower than in circulating blood. As you can see that even under these very conservative assumptions, 480 mg results in a CD16A occupancy in the tumor that is sufficient for maximum NK cell activation. In summary, as stated on slide 17, our decision for 400 mg as a recommended phase II dose is based on the good safety profile and the PK and PD data that I just showed. As next steps, we plan to open the expansion cohorts at 480 mg to explore antitumor activity in three selected indications. In parallel, we also plan to continue dose escalation of AFM24 to 720 mg. The cohort is currently open for patient enrollment to gather additional safety data and provide the basis for alternative scheduling, like a once every two or once every three application of AFM24. If we now turn to the two combination studies, namely the combination with NK cells, autologous NK cell AFM24-103, and the combination study with atezolizumab AFM24-102. For both of these trials, the starting dose of AFM24 will be 160 mg, followed by dose escalation steps, through which we will assess safety and identify a recommended phase II dose for the combination. These recommended phase II doses will then be used in the dose expansion phases, which, as I described, will follow Simon two-stage design in five of the six cohorts, with interim analysis after 12-18 patients and the ability to enroll up to 40 patients. On slide 18, you see the design of the 102 study where we combine AFM24 with atezolizumab. In this trial, we will focus on non-small cell lung cancer, gastric cancer, and hepatobiliary pancreatic cancer, all areas of very significant unmet medical need. The cohorts in non-small cell lung cancer and gastric cancer follow the described Simon two-stage design. The third cohort that can include hepatocellular cancer, biliary tract cancer, and pancreatic cancer is designed as a signal identifying basket cohort with descriptive statistics. If we move to slide 18, here we show the design of our study, AFM24-103 combination of AFM24 with adoptive NK cell transfer. This study will focus on non-small cell lung cancer, colorectal cancer, and head and neck cancer. We will use this innovative approach in these indications where patients' endogenous NK numbers are dysfunctional or only exist in insufficient numbers has a good opportunity to show activity. In contrast to the AFM24-101 study, where we also evaluate CRC but require previous treatment with EGFR antibodies, and thus will most likely exclusively recruit CRC patients with KRAS wild type. The CRC cohort in AFM24-103 will focus mainly on patients with KRAS mutations. Finally, on AFM24, you may have seen the presentation at the most recent Triple Meeting where we showed that AFM24 enhances cytotoxicity against EGFR-positive tumor cells when combined with SNK01, the autologous NK cell product. The addition of AFM24 to autologous SNK01 cells improved cell killing when compared to NK cells alone in EGFR-positive tumor cell lines, regardless of EGFR mutational status. To summarize on slide 19, the status of the AFM24 program, we are very excited that we can now embark on a broad development program with several indications with significant unmet medical need. These studies, as shown, will generate a continuous flow of data in 2022 and beyond. With that, I will turn the call over to my colleague, Arndt Schottelius, who will present our novel fully owned ICE AFM28. Arndt, please. Thank you, Andreas, and also for me, good morning, good day, everybody. Warm welcome to the call. I'm really excited to introduce AFM28 to all of you, which is our newest addition to our portfolio. As shown on slide 21, we recently announced our newest innate cell engager, AFM28, which is designed to bind CD123, an established target in myeloid malignancies. We chose CD123 as it is almost universally expressed on leukemic blasts and leukemic stem cells in patients with AML, both at diagnosis and at relapse, independently of cytogenetic risk. AFM28 is being developed for the treatment of patients with acute myeloid leukemia. We believe that AFM28 could be the key to novel treatment approaches that can fulfill several unmet needs. I would like to spend a few minutes to explain this and lay out why we are so excited about adding AFM28 to the arsenal against leukemia. AML is the most common form of adult acute leukemia. More than 40,000 patients are diagnosed with this disease every year in the seven major markets. The outcomes have remained very poor, and treatment options are generally limited, particularly for relapsed or refractory disease. As shown on slide 22, in AML, most patients become refractory to standard induction treatment or relapse within one year. Only one of three patients is alive after one year once they become relapsed or refractory, and after five years, it is only one out of 10 patients. It is obvious that new drugs are needed that reduce the high rates of relapse or prolong the time to relapse by inducing deeper responses and by eradicating measurable residual disease or MRD. In addition, for patients who have relapsed or are refractory to standard treatment, alternative options to induce remissions that are long-lasting are urgently needed. This all needs to be achieved for a patient population that is elderly. Note that over 80% of patients are over 60 years old and can often not tolerate treatments associated with toxicity. These new approaches not only need to be more effective, they also need to be safer. Recent data have demonstrated that natural killer cell-based innate immunotherapy is emerging as a promising treatment option in AML based on the demonstrated susceptibility of leukemic blasts for NK cell killing and clinical activity of allogeneic NK cell therapy in relapsed refractory disease. Also, these treatments are remarkably well-tolerated, yet these approaches rely on the cell's natural ability to recognize leukemic cells, so these cells are not specifically targeting against the tumor. Immune evasion from NK cell killing is a well-known phenomenon, and escape of leukemic stem cells in AML has been described. To effectively deplete leukemic cells, including leukemic stem cells, a targeted approach, in addition to natural cytotoxicity, has the potential to induce more frequent and deeper responses. We believe these statements are also supported by the data that we have generated with AFM13 in combination with NK cells. We designed AFM28 to be differentiated versus available therapy and to bring a truly novel approach to the treatment of AML. As we show on slide 23, AFM28 binds with high affinity to both CD123 and CD16A, and no such molecule currently exists to our knowledge. It thereby strongly activates NK cells, inducing ADCC, and through binding to CD123, causes depletion of leukemic blasts and leukemic stem cells. We will be presenting preclinical data for AFM28 at ASH and plan to submit an IND application in the first half of 2022 and to start a clinical study in the second half of 2022. With that, I'll hand the call over to Angus to review the financials. Angus? Thank you, Arndt. Affimed's consolidated financial statements have been prepared in accordance with IFRS, as issued by the International Accounting Standards Board or IASB. The consolidated financial statements are presented in euros, which is the company's functional and presentation currency. Therefore, all financial numbers that I will present in this call, unless otherwise noted, will be in euros. We ended the third quarter of 2021 with cash and cash equivalents of EUR 198.7 million, compared to EUR 146.9 million on December 31st, 2020. Based on our current operating plan and assumptions, we anticipate that our cash and cash equivalents will support operations into the second half of 2023. Net cash used in operating activities for the quarter ended September 30th, 2021, was EUR 25.6 million compared to EUR 3.6 million in the third quarter of 2020. Total revenue for the third quarter ended September 30th, 2021, was EUR 8.7 million compared to EUR 10.5 million for the quarter ended September 30th, 2020. Revenue for the third quarter of 2021 mainly comprised of collaboration revenue from Genentech and Roivant. Research and development expenses for the third quarter of 2021 was EUR 20.6 million compared to EUR 10.1 million for the third quarter of 2020. The increase in R&D expenses compared to the same period last year were driven primarily by increased expenses for AFM24, including costs for the production of clinical trial material, an increase in costs associated with other early-stage programs and infrastructure, and an increase in share-based payment expense. General and administrative expenses for the third quarter of 2021 were EUR 6.8 million compared to EUR 3.5 million in the quarter ended September 30th, 2020. The increase relates largely to higher personnel expenses, higher premiums for insurance, higher consulting expenses, and increased share-based payments. Net finance income for the quarter ended September 30th, 2021 was EUR 1.5 million compared to net finance loss of EUR 3.1 million in the quarter ended September 30th, 2020. Net finance income loss is largely due to foreign exchange gains or losses related to assets denominated in U.S. dollars as a result of currency fluctuations between the U.S. dollar and the euro. Net loss for the quarter ended September 30th, 2021 was EUR 17.1 million or EUR 0.14 per common share, compared with a net loss of EUR 6 million or EUR 0.07 per common share for the quarter ended September 30th, 2020. The weighted number of common shares outstanding for the quarter ended September 30th, 2021 was EUR 119.8 million. With that, I'll turn the call back to Adi for closing remarks. Adi. Thank you, Angus. As you've heard now, we have made continuous progress with our two lead programs, AFM13 and AFM24, and soon we plan to have a third innate engager that we're presenting called AFM28 in the clinic. As we now look ahead, as shown on slide 24, we expect the rest of this year and 2022 will be busy as we have numerous clinical trials from which we expect to report data. Our expected key milestones are as follows. For AFM13, we will host an investor event in December, where we plan to provide a data update on our ongoing trial in combination with natural killer cells. In addition, for AFM13 monotherapy in peripheral T-cell lymphoma, we expect to complete enrollment in our registration-directed study in the first half of next year. We've broadly explained where we stand with AFM24, and for monotherapy, we are now planning to open the expansion cohort before the end of this year. There is an abstract with data from the dose escalation for presentation at American Medical Conference in the first half of 2022. As we move forward with the expansion cohort to report the initial data in 2022. We have set up two additional studies for AFM24 in combinations either with natural killer cells or with anti-PD-L1 atezolizumab. We are expecting to complete the first dose escalation cohort in each study during the first half of 2022, start with the dose cohort expansion if safety is favorable, and thereby also be able to provide updates as we progress. For AFM28, a very new candidate that we carefully selected in order to address the high medical need. After the ASH data update, now our next milestones are the planned IND submissions in the first half of 2022, and subsequently, the initiation of clinical studies. We're planning again, as explained before, to do this in monotherapy and also, combinations, in particular, in combination with natural killer cells. We are preparing the company to meet these opportunities and look forward to bringing innovative medicines to patients that need them. Now, on behalf of the entire team, I would like to once again express my gratitude to everybody who is contributing to these efforts. We're now ready to take any questions that you may have. Operator. Certainly. Ladies and gentlemen, once again, if you have a question, please press star then one. Our first question comes from the line of Daina Graybosch from SVB Leerink. Your question please. Hi. Thank you for the question. Just looking at the data that you presented on AFM24, maybe a two-part question. Can you remind us why you think these three planned expansion cohorts will be most amenable to single-agent activity, so the CRC KRAS wild type, the EGFR mutant lung, and the RCC? Then it is, I guess, those tumor types where you did see this, the stable disease or that patient with progressive disease that continues on treatment. Can you share anything more about those patients? Do they have a high EGFR expression? Were they refractory to other EGFR-targeted therapies? Thank you. Thanks, Daina. I'll hand this over to Andreas, please. Hi, Daina. Let's start with probably the second question or second part first. The patients that we have treated on 480 mg, we have these two patients with EGFR mutant non-small cell lung cancer and colorectal cancer patients. Important to note, we decided which tumor types will go into which of the studies prior to seeing the data. As I said, this decision was really driven on this comprehensive analysis that we showed, where we looked at data from more than 10,000 patients and then really looking at biology of the innate immune system, activating and inhibiting factors in NK cell biology. What we see now here on slide six, again, very small and on the cohort six, very small patient numbers. It's a little bit maybe an early confirmation of our selection process. If you look at the colorectal cancer patients, wild-type patient number one, this would be a patient who would have qualified for the expansion cohort. Patient number three, EGFR mutant non-small cell, another patient that would have qualified. Patient five, again, EGFR mutant, would be a patient that would have qualified. The other two patients, two and four, where we have follow-up data, patient six is very early in his treatment, would have not qualified for the expansion cohort as monotherapy. Again, the sequence was different. We looked at the biology first and then decided which are the most likely cohort or most likely tumor types that can respond. Again, with this very small data set there seems to be a trend that exactly these tumors really do quite well on AFM24 monotherapy. Now, we have measured EGFR across all cohorts. Most patients have moderate to high expression. I do not have the individual patient numbers or data, but I would expect EGFR mutant non-small cell lung cancer patients have rather high expression of EGFR receptor. As a requirement, they needed to exhaust all previous lines of therapy, so all of these patients have been pretreated and have become resistant to EGFR-targeting therapies, whether it's TKIs or antibodies. Very helpful. Thank you. Thank you. Our next question comes from the line of Maury Raycroft from Jefferies. Your question please. Hi, good morning. Good day, everyone, and congrats on the updates, and thanks for taking my questions. I had a question on AFM24-2. For that one, you showed a lot of helpful PK and PD data. I'm wondering if you can tie it together with what you're seeing in the six patients at 480 mg, particularly in respect to antitumor activity as you approach steady state. If you can talk more about what you're seeing on cytokines and NK cell activation markers as exposure increases. I can take the first part. Let me hand over to Arndt regarding the cytokines. Yeah, as you see, these patients are treated at 480 mg. This is the dose level where we achieved dose proportionality. We have basically saturated EGFR binding. As we showed, we also achieved CD16A receptor occupancy and then correlating figures in the tumor that, according to our experiments, are sufficient to maximum activation of the tumor-residing NK cells. We have not broken down this data on an individual patient level yet, but this is something that we will have to do in the future. And maybe- Arndt, maybe you can talk. Yes. on the NK cell. Yeah. Mm-hmm. Yeah, sure. Happy to do so. You noted, Maury, we didn't share that data because we want to disclose that, as discussed at an upcoming conference in 2022. What we see, what I can share with you in terms of the cytokines, to give you an example, interferon gamma, TNF-alpha, important for NK cell activation at doses at or above 160 mg. When we look at the steady-state levels, we see a steady increase. We didn't see a real difference between 320 mg and 480 mg, but we see that it clearly was rising above 160 mg, making the point again that this is clearly pharmacologically active. In terms of the activation markers, similarly, we want to share that data when it's also a little bit more matured. The same trend that we see at doses above 160 mg, we saw an increase of those activation markers, again, showing that we have consistent, NK cell activation. Hopefully that helps with your question. Yep. Yeah, that's very helpful. Maybe one other question on the AFM13, plus cord blood NK cell combo study. Just wondering if you can talk more about expectations on durability, for this upcoming update. Also just checking if you have plans to move this study over to sponsorship at Affimed at some point. Andreas, can you take the question, please? Yeah. What you see or what you realize is, when you compare to the status that we have basically by the middle of the year, June or so, we have added a very significant number of patients over the last couple of months. I would say that for the highest dose cohort, time to progression or duration of response data will be quite immature in December as many of these patients have recently started treatment within the last three, four months. Of course, on the lower doses, we have a longer follow-up, but again, this will not be the therapeutic doses that we will move into our expansion cohort and will use subsequently. Now in terms of sponsorship, we have not decided. As we always said, we are working on with several CDMOs to transfer the production process. We are in the process of doing that, and we'll provide updates as we have more concrete data to share. Got it. Okay. That's helpful. Thanks for taking my questions. Thank you. Our next question comes from the line of Kripa Devarakonda from Truist Securities. Your question please. Hey, guys. Thank you so much for taking my question and congrats on all the progress. I have a follow-up question on the AFM13, the cord blood NK cell combo. Can you talk a little bit about the decision to expand into both HL and NHL patients? What should we expect the split to be? Are you looking to enroll more NHL patients? Maybe talk a little bit about how this, if at all, this changes your strategy in what to focus on, whether it's HL or NHL. Thank you so much. Thanks a lot, and a gain, I'll have Andreas answering your question. Andreas? Yeah. As you know, CD30 is a target that is expressed on Hodgkin's, but also on non-Hodgkin's lymphoma, like T-cell lymphoma or subset of CD30-positive B-cell lymphomas. Currently we are following, if you will, a two-pronged approach. Clearly our main indication, or the first indication, I would say, will be Hodgkin's lymphoma where we have the wealth of data and where we have seen these very impressive responses already in the first four patients. This is, the study is now designed that it will recruit 30 Hodgkin's patients at the recommended phase II dose, which we believe gives us good data set to move on with Hodgkin's on the registration path. Now the second part is a little bit opportunistic. Again, there's also very significant medical need in peripheral T-cell lymphomas and in diffuse large B-cell lymphomas. We thought that we at least should explore NK cell-based, AFM13-based combinations in these diseases that could potentially result in a second or a third development pathway. This is really broadening the indications. For now, Hodgkin will be our lead indication where we will try to move ahead with full steam. Great. Thank you. Just a follow-up question on the AFM24, the data that you presented. Now you've been dose escalating for a while, but have you seen any indication, especially with the lower doses where patients have been treated for a longer period of time, a deepening of responses? Andreas? We have occasionally seen some disease stabilization at the lower doses. Again, according to our data, the maximum pharmacokinetic/pharmacodynamic activity was set in around 160 mg-320 mg, with 480 mg being our selected dose right now. These are really anecdotal observations. As we said, out of our 480 mg cohort, four of six patients are still on treatment. I think this will be interesting cohort to watch whether we do see a deepening of responses. Great. Thank you very much. Thank you. Our next question comes from the line of Nick Abbott from Wells Fargo. Your question please. Good morning. Thanks for taking our questions, and thank you for all the detail on AFM24. First question is on AFM28. You know, can you speak to why CD133 in the context of a CD3, CD33 engager you built for Amphivena. You know, compare CD123 to CD33 and NK cells to T-cells, you know, in this application in AML. Thanks. Yeah, I'm happy to take this question. Arndt? Yes. Happy to do that. Nick, yes, I think we already also provided some background information. As you rightly said, Amphivena has this CD33, I think a very valid target, of course, in combination with a CD3, the T-cell engager. Why have we selected, maybe let me speak about or reiterate CD123. One is it is very broadly expressed on the leukemic blasts. It's also expressed on leukemic stem cells and, importantly, not on healthy stem cells. So we have a very high selectivity. We've also followed our approach in selecting this when we look at, in a way, programs that have been out there, like an Fc-enhanced CD123-targeting antibody that comes from Johnson & Johnson a while ago, Talacotuzumab, that was not continued because as an Fc-enhanced antibody without the additional mechanisms of action that we believe we add in terms of also the efficacy, in terms of the, let's say, tuning engineering with the molecule, we see a great potential to address that medical need. Indeed, also with those approaches, Talacotuzumab, the occasional complete responses were seen. Where we are specifically excited is in the prospect, of course, testing monotherapy that, but then very quickly combining AFM28 with allogeneic NK cells. Why? Because we know in AML, of course, a myeloid disease, NK cells and macrophages will not be fully functional or not functional. Adding, in a way, you could say the payload or mechanism of action with allogeneic NK cell transfer, we see a very high probability of success to getting to those deep responses that we're looking at, which is this very high medical need to really get to also minimal residual disease negative patients. Hopefully that kind of addresses your question, Nick. Yeah. I think I guess the point of NK cells, T cells emphasizes the safety advantage you feel there is with an NK cell versus a T-cell engager. Yes, absolutely. That is an important point. We have now seen consistently across our NK cell engagers excellent safety profile. I mean, some of the early IRRs that we have seen very well manageable scheduled pretreatments. NK cells are just by the nature of their biology, very effective, but much safer than T cells. Again, I think we know the principle by now. It's not only the cytokine storm, but it's also really the, in a way, autoimmune effects that we see where T cells once unleashed are just not selective in kind of targeting or attacking the tumor versus healthy tissues. Whereas NK cells very well distinguish clearly, thus a very much better safety profile. As I laid out, I think when you look at the very elderly patient population that we have, frail patients that will not tolerate some of them high-dose chemotherapy, we see this as a very differentiated good profile with an NK cell engager. Terrific. Maybe just last one from me. You know, in solid tumors, obviously with AFM24, you've described very elegantly the three-prong strategy. You've already alluded to an NK cell combo. For AFM28, at least two prong, is there a three-prong strategy that you think that's applicable for AFM28 myeloid disease? That's a really good question. Happy also for Adi or Andreas to jump in. We have currently, you know, also publicly said we want to make the combination with allogeneic NK cells a priority because of the reasons I've been giving. There may be cases for also the kind of third pillar. That's not something that we have fully thought through and would update accordingly as we move on with our plans. Terrific. Thank you very much. Thank you, Nick. Thank you. Our next question comes from the line of Brad Canino from Stifel. Your question please. Thank you and appreciate the updates today. Just quickly on the protocol amendment for AFM13 NK, was that driven by MD Anderson or by your team? If you could talk more about the reason behind that. I'm also interested in the breakdown of the six AFM24 patients you had at the 480 mg cohort. You highlighted how three of these would have been eligible for the monotherapy expansion cohort, but they had, you know, four to seven prior lines of therapy it looks like. In the expansion cohort, should we expect this number of prior lines of therapy, or will you be looking for patients that, you know, may be earlier at one or twp prior lines? Thank you. I guess, Andreas, both questions are for you. Yeah. Yeah. Let's start with the amendment of the protocol. I think we have a very good, very close working relationship with MD Anderson. I would say it was basically a joint effort, joint decision. Initially the protocol was only designed to evaluate safety, so it was a pure phase I safety protocol. Then I would say even for us, a little bit unexpectedly, we saw this really significant antitumor activity already at the lower dose levels. We immediately developed the desire to gather more efficacy data and to basically put this compound on a development path. We use the existing protocol to allow for more patients at the recommended phase II, which will give us sufficient number of patients to really have a good solid estimation of efficacy in Hodgkin lymphoma. As we always said, will provide us the basis to engage with healthcare, with regulators for the most appropriate and the fastest path towards approval. This was a joint decision, and it was really driven by our enthusiasm both MD Anderson and our enthusiasm about the data that we were seeing. Now in terms of the expansion cohorts in study 101, yeah, you are right, these patients are heavily pretreated. I think taking this into account of seeing this degree of activity in late line at least for us is really very encouraging. Whether there will be less pretreated patients in the expansion cohort is a little bit hard to say. The expansion cohort still require that patients have exhausted all available treatment options for their respective diseases. I would say we will see a majority of patients with three to four lines of previous therapy. Again, we are acting here in an area of a very significant unmet medical need, which generates a higher bar. On the other hand, we believe also sets the scene for a potential accelerated approval process if you can show robust and reproducible activity in patients that have no treatment alternatives left. Thank you.