Good day, and welcome to Affimed's second quarter 2021 financial results and corporate update conference call. I'd now like to introduce your host for today's conference call, Alexander Fudukidis, Head of Investor Relations at Affimed. Please go ahead. Thank you, Liz. I'd like to also welcome you all for joining us today for our second 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, and Angus Smith, our Chief Financial Officer. The whole team will be available for the Q&A session. Before we start, quickly to 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 the statement. 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 Statement in the press release that we issued today and filed with the SEC. With that, I'll turn the call over to Adi. Adi? Thank you, Alex, and good morning, everyone. Thanks a lot for joining in for our second quarter update call. Today, we're going to provide an update on our pipeline, discuss the progress on our ongoing AFM13, AFM24, and AFM28 studies and our plan for what promises to be an exciting period over the next few months for our company. Before I do that, a quick summary of what we have accomplished so far. The clinical and pre-clinical data confirm that our unique and innovative innate cell engagers are safe and have the potential to be effective in treating cancer patients, both as monotherapies but also in combination either with natural killer cells or with checkpoint antibodies such as PD-1, maybe PD-L1. As we move the ongoing clinical trials forward, our efforts are now focusing on identifying and targeting indications where we believe our scientific discoveries will benefit patients by applying our three-pronged approach: monotherapy, therapies in combination with natural killer cells, and checkpoint inhibitors. We're very happy to report that our pipeline remains on track for our registration-directed study of AFM13 monotherapy in relapsed refractory peripheral T-cell lymphoma. We are recruiting well and on track to complete enrollment of the study in the first half of 2022. We expect to be able to provide further guidance about timing for data as we get closer to the completion of enrollment. In the investigator-sponsored clinical trial at MD Anderson Cancer Center, evaluating cord blood-derived natural killer cells pre-complexed with AFM13, we have completed the dose escalation part of the study with increasing doses. Indeed, there were three cohorts where we used either 10 to the 6 cells per kg, three patients that received 10 to the 7 cells per kg, and three patients that received 10 to the 8 cells per kg. We're currently enrolling additional patients at the highest dose of 10 to the 8 cells per kg to gather robust data on safety and efficacy, what would form the basis for discussions with regulators about appropriate approval strategies. No dose-limiting toxicities have been observed during the dose escalation in any of the three cohorts, and we remain encouraged by the observed response rates. The next data update is planned for the fourth quarter at a major medical conference. Regarding our efforts to take forward the combination of AFM13 with natural killer cells into a registration direct study, we have signed up a CDMO for the manufacturing of the NK cells and have generated additional data on cryopreserved natural killer cells pre-complexed with AFM13. As we have shared with you over the past few months, we view this CAR-like NK characteristics of our innate cell engagers in combination with natural killer cells as a major advantage over monoclonal antibodies. The major difference being that when we look closer at the cell surface retention, our innate cell engagers won't fall off in combined therapy for a very long time, including days later. Whereas monoclonal antibodies are not retained for very long. As a result, our research shows that it is not possible to generate a pre-complex product with monoclonal antibodies, but with innate cell engagers only. Moreover, our research demonstrate that the engagement of our innate cell engager molecules with natural killer cells activate the natural killer cells to kill tumor cells. In our collaboration with the Karolinska Institutet, we found that AFM13, when compared to a monoclonal CD30 antibody, mediated a more potent activation of natural killer cells, leading to a significantly increased number of natural killer cells that exerted engagement with multiple target cells, rendering these NK cells serial killers. This exciting data has been accepted as a poster presentation at the SITC annual meeting in November. In our ongoing trial with MD Anderson, it is our goal to generate a strong data package that would support discussions with the FDA and other agencies regarding next steps for the program, including a potential registration-directed study. Now let me turn over to AFM24, our EGFR-directed innate cell engager. For AFM24, we continue to execute our three-pronged strategy of monotherapy, combination with natural killer cells, and combination with a checkpoint inhibitor PD-L1. Our goal in this program is to evaluate a broad set of solid tumor indications in parallel, supported all by a strong biological rationale. We expect multiple inflection points this year and plan to have multiple additional data readouts in 2022. Our monotherapy dose-escalation study is on track. Based on current cohorts five and six are pharmacologically active doses. Therefore, we have increased the size of cohorts five, patients are dosed at 320 mg, and cohort 6, patients are dosed at 480 mg, to generate additional pharmacokinetic and pharmacodynamic data that we expect will aid our selection of the recommended phase II dose. As of today, in each of cohorts five and six, five out of six patients are enrolled. It is important to mention that to date, in patients that have already completed the DLT period in each cohort, no dose-limiting toxicities were observed. As just mentioned, we continue to see a good safety profile of AFM24. We confirm that we have not seen any of the classically EGFR-related side effects like acneiform, skin rash, or mucositis. This is in line with the distinct mechanisms of action of AFM24, which is very different from the mode of action of EGFR pathway-targeting antibodies like cetuximab or panitumumab. These findings also confirm the data from our pivotal toxicology studies in cynomolgus monkeys that indicated a different side effect profile for AFM24 versus cetuximab. Infusion-related reactions remain the main side effect and are well manageable with symptomatic treatment and modifications of infusion rate. The ongoing dose-escalation part includes patients with any EGFR expressed in solid tumors. When assessing antitumor activity at those levels in the 320 mg and 480 mg cohort, we are encouraged to see that there were several patients on the study that experienced disease stabilization beyond eight weeks and were able to receive additional cycles. Biomarker analysis of the patients point to the activation of effector cells, shown by increasing expression of activation markers and a continuous secretion of cytokines. In support of this observation is a continuous occupancy of the CD69 receptor. Independent of the selection of our recommended Phase II dose, we plan to continue to increase the dose in non-selected patients to gather further insight into the exposure-effect relationship of AFM24, focusing on PD markers, and to confirm safety of AFM24 at even higher dose levels. Important now to note is, in addition, in line with our guidance, we expect now to start enrollment of indication-specific patients in the expansion cohorts using single-agent AFM24 in the second half of 2021. These cohorts have been chosen based on a detailed analysis of the tumor biology, as we explained in the past, and will enrich for patients that we believe have a high likelihood to respond to single-agent AFM24. These expansion cohorts will include renal cell carcinoma that failed standard of care, which includes TKIs and PD-1 targeted therapy. Second indication is non-small cell lung cancer, EGFR mutant, failing standard of care TKI. The third indication is colorectal cancer failing chemotherapy plus EGFR-targeted antibody. We have selected three indications for the monotherapy study. We are now in the final stages of the setup phase for our combination studies of AFM24 with both atezolizumab, study is called AFM24-102, and the autologous NK cell product SNK01. This study is called AFM24-103. We confirm our guidance that we expect both of these studies to start enrolling patients in 2024. The tumor types we plan to study with the AFM24 atezo combination are as follows. Non-small cell lung cancer, in this case, EGFR wild type, failing chemo and PD-1 targeted therapy. Gastric and GEJ cancer failing standard platinum-based chemo, and a basket of EGFR-expressing tumors comprising pancreatic, hepatocellular, and biliary tract cancer, failing standard of therapy for the respective disease. The tumor types we plan to study in the AFM24 SNK01 NK cell combination study are as follows. Again, non-small cell lung cancer, EGFR wild type, squamous cell carcinoma of the head and neck, failing chemo and PD-1, and colorectal cancer, failing standard of care. The indications for each of the three studies have been selected carefully based on the biology of each tumor type. This approach allows us to investigate a broad set of solid tumors while also providing multiple shots on goal for the more prevalent tumor types, such as non-small cell lung cancer and colorectal cancer. In summary, we're very satisfied with the progress of the AFM24 program. The data show that AFM24 possesses a different mode of action compared to conventional EGFR-targeting antibodies. We see pharmacological activity based on CD16A receptor binding and NK activation markers. At these pharmacologically active doses, we see no classical EGFR-related side effects like skin mucosal toxicity. In addition, we are seeing disease stabilization in these heavily pre-treated patients at those levels 320 mg and 480 mg. We believe in the significant potential of AFM24, and with the planned expansion of the program, we're seeking to maximize this opportunity, addressing a broad set of major EGFR-expressing tumor indications. This strategy will allow us to provide a continuous flow of data. Now let me move to the third program, AFM28. For AFM28, we continue to advance the IND-enabling studies and have submitted an abstract with initial preclinical data for a major medical conference later this year. We plan to release information about the target and the indication once the abstract becomes available. We remain on track to submit the IND application in the first half of 2022, and our goal is to begin a clinical study in the second half of 2022. In addition to moving things forward in the clinic, we're continuing to publish data that supports our work. One such example is the recently published preclinical data that supported the IND filing, IND application of our innate cell engager AFM24 in the journal, mAbs. Arndt, our CSO, will discuss the key takeaways from the publication. Arndt? Thanks, Adi, and also from me, a very warm welcome to everybody on the call. As introduced by Adi, I would like to summarize the key preclinical data for AFM24 described in the recent publication in the journal, mAbs. In this paper, we demonstrate the high-affinity binding of AFM24 to CD16A on natural killer cells and macrophages with strong binding values in the low nanomolar range. Importantly, AFM24 binds to CD16A on NK cells and macrophages with high affinity at a site that is distinct from binding of IgG, such that high concentrations of polyclonal IgG results in a minimal, only twofold reduction in binding affinity. In contrast, binding of an Fc-enhanced high-affinity anti-EGFR IgG antibody was significantly inhibited. These data again demonstrate the high surface retention of our ICE molecules to NK cells, enabling the earlier described pre-complexing to NK cells with CAR-like NK cell properties, which are not possible with normal or Fc-enhanced antibodies. We also show high-affinity binding of AFM24 in the nanomolar range to various EGFR-expressing tumor cells. AFM24 demonstrated to be highly differentiated from marketed anti-EGFR antibodies with its ability to potently and effectively kill tumor cells. Through antibody-dependent cell-mediated cytotoxicity, or ADCC, by NK cells. This ICE-mediated potent antibody-dependent cellular phagocytosis, or ADCP, via macrophages in vitro. AFM24 was also shown to be effective towards a variety of EGFR-expressing tumor cells, killing these regardless of their EGFR expression level and irrespective of their KRAS or BRAF mutational status. In addition, as AFM24 has a lower affinity for EGFR and binds to a different epitope than cetuximab, it exerts an over 1,000-fold lower inhibitory activity on EGFR signaling, further underscoring its highly differentiated mechanism of action. In terms of in vivo data, in tumor mouse models, we have published at AACR, this year's AACR, showing dose-dependent antitumor activity of AFM24 in combination with freshly isolated NK cells. This antitumor activity for AFM24 in combination with NK cells has now also been demonstrated with pre-complexed and cryopreserved NK cells in vitro and in vivo within one of our preclinical collaborations. This exciting data gives us confidence that the NK cell product we use in combination with AFM24 retains its potent antitumor activity after cryopreservation in vitro and in vivo. Now coming to the toxicology studies in cynomolgus monkeys, also described in the paper, AFM24 was well-tolerated up to the highest dose of 75 mg per kg when administered once weekly for 28 days. Remarkably, skin and other toxicities which had been observed at these dose levels with cetuximab in comparable cynomolgus monkey studies were not observed here. Only transient elevation of interleukin-6 levels was detected at all dose levels, which returned to baseline after 24 hours. Moreover, an increase in circulating CD14 monocytes was observed after the first dose of AFM24, concurrent with a decrease of circulating NK cells at doses of greater or equal to 80 mg per kg. In all views showing the expected pharmacodynamic effect of this drug candidate. Taken together, these results emphasize the promise of our bispecific NK cell engagers as an alternative cancer therapy and demonstrate the potential for AFM24 to effectively target tumors expressing various varying levels of EGFR, regardless of their mutational status. Happy to answer any questions you may have about this in our Q&A. For now, I'll hand the call over to Angus to review the financials. Angus? Thank you, Arndt Schottelius. 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 entered the second quarter of 2021 with cash and cash equivalents of EUR 222.7 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 June 30th, 2021, was EUR 17.3 million compared to EUR 15 million in the second quarter of 2020. Total revenue for the second quarter ended June 30th, 2021, was EUR 9.7 million compared with EUR 2.9 million for the quarter ended June 30th, 2020. Revenue for the second quarter of 2021 mainly comprised collaboration revenue from Genentech and Roivant. Research and development expense for the second quarter of 2021 was EUR 21.8 million compared to EUR 11.7 million for the second 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, as well as an increase in costs associated with our other early-stage programs and infrastructure and an increase in share-based payment expense. General and administrative expenses for the second quarter of 2021 increased by 109% to EUR 5.4 million from EUR 2.6 million in the second quarter ended June 30th, 2020. The increase relates largely to higher personnel expenses, higher premiums for our directors' and officers' liability insurance, higher consulting expenses, and increased share-based payment expenses. Net finance costs for the quarter ended June 30, 2021, increased by 63% from $1 million in the quarter ended June 30, 2020, to $1.6 million during the second quarter of 2021. The increase is largely due to foreign exchange losses related to assets denominated in US dollars as a result of the weakening of the US dollar against the euro during the quarter. Net loss for the quarter ended June 30, 2021, was EUR 18.8 million, or EUR 0.16 per common share, compared with a net loss of EUR 12.2 million, or EUR 0.16 per common share, for the quarter ended June 30, 2020. The weighted number of common shares outstanding for the quarter ended June 30, 2021, was 119.6 million. I will now turn the call back to Adi for closing remarks. Adi? Thanks a lot, Angus. As just explained, our company is making significant strides forward by advancing science and demonstrating that our innate cell engagers can play a leading role in enabling innate immune cells to identify and eliminate cancer cells. Now, for AFM13, our development strategy allows us to target a broad set of CD30-positive lymphoma, indeed, including various types of non-Hodgkin and Hodgkin lymphoma. We're very excited about the potential and market opportunity for AFM13 in these indications, and we will have additional data for the NK cell combination study by the end of the year. For AFM24, we're now executing a strategy that we believe gives us the highest probability of success. We have reached active dose levels in our dose escalation study and will now use this to initiate this three-pronged development approach in parallel, indeed, across a broad set of solid tumor indications. We expect that these three studies will generate a continuous flow of data. Finally, we are executing on our pre-candidate pipeline to bring additional product candidates into the clinic. Our development progress for AFM28 is indicative of our ability to further expand our pipeline by leveraging the unique ROCK platform, and we're working on additional early candidates from the platform. Many people have contributed to bring our innovative therapies to patients who need additional options in their fight to cancer. These include patients and their families who entrust us with the lives of their loved ones, our employees, and the investors, who over the years have supported our efforts. As always, I'm very thankful for the trust you put into our efforts. Thank you. We're now ready to take any questions that you may have. Operator? Ladies and gentlemen, if you'd like to ask a question at this time, please press the star, then the number one key on your touchtone phone. To withdraw your question, press the pound key. Our first question comes from Daina Graybosch with SVB Leerink. Hi, all. Thanks for the question and for the pretty nicely comprehensive call. 2 for me on AFM24. The first is, I believe you mentioned, I just want to confirm, that you saw stable disease in several patients beyond eight weeks. In that same sentence, you mentioned that you were recruiting any EGFR-expressing solid tumors. I'm wondering if you could clarify whether you saw the stable disease in patients that had more EGFR expression. Was there any correlation with that? Even if you could tell us of these patients recruited at cohorts five and 6, what proportion of them did have high EGFR and which ended up with low EGFR? That's the first question. The second question is, can you confirm how you ultimately will select a dose, given you haven't hit any dose-limiting toxicity? Will you be going off pharmacodynamic activation in periphery? What gives you confidence that that will track with your activity in the tumor? Will you be going off of occupancy of CD16 or EGFR, or will you continue to try to dose as high as possible till you do understand your highest tolerable dose? Thank you very much. Thank you, Daina. I have to check if Andreas is still on the phone. Andreas, could you follow? I'm- Specific questions and okay, very good, Andreas. I'm on the phone. I apologize. I'm in rural Italy, so if I break up at some point, it's due to technology reasons. I try to stay as long as I can. Let's start with the second part of the question first, and Arndt also chime in. As we always said, the selection of our recommended phase II dose will be based on pharmacodynamic markers. As Arndt mentioned, our mechanism of action is completely different from EGFR pathway-targeting agents like cetuximab or other TKIs. We were not expecting to see any dose-limiting toxicity like skin or mucosa. What in fact seen clinically is really reconfirming this assumption. IRRs remain the side effect, which are well manageable, but we are not seeing any skin toxicity, any mucosal toxicity. As we said, in terms of pharmacodynamic markers, we have a whole array of parameters that we look at. The most leading parameters are markers of the activation of circulating NK cells, as well as the occupancy of the CD16A receptor, where we see values that are well above those values needed for experimental activity in vitro and in vivo. We feel very confident that we are currently working at pharmacodynamically active doses. This is our doses that we will take forward into phase II testing, both as a single agent as well as in combinations. Irrespective of this, we may escalate 1 or 2 additional dose steps just to confirm that we have a very good safety profile, a very good safety window, but not necessarily to use these higher doses for further evaluation of clinical activity. In terms of EGFR expression, we are collecting the data. Again, for the highest dose levels, we have not all data in-house. For the lower dose levels, we could not see any correlation between the degree of EGFR expression and any of the clinical parameters. Again, the data for the two highest dose levels in terms of EGFR quantification are still pending. Got it. Thank you very much. Our next question comes from Maury Raycroft with Jefferies. Hi. Good morning, everyone. Good afternoon. Congrats on the progress. Thanks for taking my questions. One question on AFM24. You mentioned additional inflection points for the program by the end of the year. Wondering if you can recap what those inflection points are. As we've mentioned, we are now planning to start the dose expansion cohorts. That's an important milestone, and we've also mentioned that there are two additional studies that are being initiated. The one is the combination study with natural killer cells, and the other one is the study with atezolizumab. These are three very important inflection points in our mind. In addition, we can provide updates as we proceed with the dose escalation study. You have heard from Andreas that we have expanded cohorts five and six to include more patients. Those data will be collected and analyzed, and once available, we plan to share this data with you. Got it. That's helpful. Maury? Mm-hmm. Yes. Yeah, I'm still here. Just wondering if you're saying anything additional about any more specifics on the activation markers and cytokine secretion that you're seeing, if you're providing any more specifics on that? Arnd? Yeah. Thanks, Maury. Good question. At this point, not specifically we would like to share that. We have said, just to repeat maybe what Andreas already said, we look at activation and exhaustion markers on circulating NK cells. We look at infiltration of the cells in some of the biopsies we have. We look at the cytokine levels. Of course, as we have reported, in addition to exposure, so PK parameters also at receptor occupancy. We will share that in more detail once all the data, as Adi also mentioned, will be collected together, and then we'll also share the specific markers used. Got it. Okay. Also wanted to ask about the AFM13 plus NK cell combo. Can you say if you have responses at the highest dose at this point, and how many patients total at the highest dose are planned for the study? We haven't disclosed any such details for the time being, as we are preparing for a presentation later in the year as outlined so that we can see the composite. In short, what the plan has been is that we have, in each cohort, initially three patients. A cohort is always a certain number of NK cells, which is increased by a factor of 10 when the safety is warranted. As I said, it's 10 to the 6 cells per kg. We move to 10 to the 7, then 10 to the 8. In these patients, we haven't seen any dose-limiting toxicities or any other side effects, so it appears quite safe. Overall, what I can say here is that we're also very encouraged by the responses that we're seeing after the first assessment. Currently, additional patients are treated. We have continued to enroll patients, or MD Anderson has continued to enroll patients at the highest dose cohort. That's currently ongoing. Got it. Okay. That's helpful. My last question, then I'll hop in the queue. In the prepared remarks, you said the program, the AFM13 plus NK cell combo program, would be robust and could enable discussions with regulators for approval strategies. Just wondering if you think you'll have enough data by year-end 2021 to enable these discussions. In terms of timing, we will let you know as soon as we have such data. It's an IST, so we're dependent on MD Anderson to enroll these patients. I would say that we have to wait for a little while before we can confirm any of these next activities. This is an important activity, but as we feel it's not the only very important activity. The other one is that we can proceed with the NK cells and its manufacturing. I was sharing two news today that we have made good progress on this front as well. First, we're now working with a CDMO for the manufacturing of the cord blood-derived NK cells, and we have generated first data of a cryopreserved AFM13 pre-complexed NK cells and determined its activity in preclinical experiment. Got it. Okay. Congrats again, and thanks for taking my question. Thank you. Our next question comes from Nick Abbott with Wells Fargo. Well, good morning, and thanks for taking our questions. Rural Italy sounds delightful, I have to say. Starting off maybe on AFM13. You mentioned the CDMO ID. Is this using cord blood from MD Anderson? Obviously, I know that you've licensed the technology from them, but are you restricted to where the cord blood cells come from, which bank they come from? Yes, we have a license to the entire technology, and this would also include, indeed, any work on cryopreservation that's being conducted by MD Anderson. In terms of cord blood cells, we're not restricted to any specific source, so we can source this from MD Anderson, but also independent places. In essence, that's how we are set up. Is there a specific reason why you're asking? No, not at all. I was just thinking, we don't know where the CDMO is, but if you were going to have a CDMO in Germany, for example, then shipping cord blood from MD Anderson wouldn't be as convenient as sourcing it from somewhere in Germany. Yeah. No, it's an international CDMO that has footprint all over the world. It's obviously one of the very experienced one that was important to us. Again, a CDMO that has already worked and developed NK cell products. We're tapping into specific knowhow already with this choice. At the moment, our focus is to work with a site in the U.S. Okay, great. Thank you. Then just on AFM24 and terrific now finally details of those expansion cohorts. One thing that struck me in the monotherapy, there's not a KRAS-mutated colorectal cohort. The NK combo would appear to allow for KRAS-mutated colorectal, but did you consider, is there a reason why there isn't a KRAS mutated cohort? Obviously, it couldn't be EGFR pretreated, and that's probably the reason, but I thought I'd ask. Andreas, can you help out here? Yeah, that's a good pick. As we said, our selection on the expansion cohorts are based on a pretty thorough analysis of the underlying tumor biology and the makeup of the different players of the innate immune system. When we look specifically at KRAS-mutated colorectal cancer, it's not due to the KRAS mutation, but there appears to be a coincidence that many KRAS-mutated colorectal cancers have very limited NK cell numbers. Then some other factors that indicated to us that KRAS-mutated colorectal cancer would be one of these indications where the patient would need support of an external NK cell source. That's the reason why they ended up basically in Study 103. We believe that once you are able to supply these KRAS mutant colorectal cancers with NK cells and with an appropriate engager, that you put the innate immune system in the best position to work against these very difficult to treat tumors. Sorry, thank you very much, and I'll hop back in the queue. As a reminder, that is star, then one if you'd like to ask a question at this time. Our next question comes from Yale Jen with Laidlaw. Good morning and afternoon, and thanks for taking the question. The first question is that for the AFM13 plus the cord blood NK cell, which that according to clinicaltrials.gov, that you have, they expect to enroll about 30 patients. Is this target still what you anticipated or has there any modification on that, and whether that potentially could be a critical mass for potential sort of registrations that discussion with FDA? Andreas, you may want to take that. Yeah. The first thing I can confirm is that the protocol is written in a way that we, in fact, can recruit somewhere between 30 and then 40 patients at the recommended dose level. This could be a mixture of Hodgkin and non-Hodgkin CD30-expressing lymphomas. Again, whether this mass or whether this number will be sufficient for any registration package, of course, will depend on the effect level. Definitely, this study will allow us, probably even earlier than going up to the full recruitment, to engage in discussions with FDA. I think during these discussions, we will learn what kind of patient numbers they are expecting. I think it's a robust study. It will give you a pretty good data set, will enable us also to look at different biologies within the CD30-expressing lymphoma space. Everything else will really depend on our initial discussions with FDA. Great. That's very helpful. A quick follow-up on this, which is that, is the data anticipated reporting at ASH or other venues? The disclosure policy is mainly driven by MD Anderson. Our expectation is that they will submit some of the data for ASH. Okay, great. Maybe one general question for the AFM24. You have the monotherapy as well as the combo, specifically with NK cell combo. I noticed that the renal cell carcinoma was only monotherapy, but not on the combo. Is there any reason behind that or maybe more specific reason behind that? Yeah. The answer is, again, it's based on the analysis of biology and the setup of the different players of the innate immune system. Clear cell carcinoma, renal cell carcinoma, we know already since we in good own time that this is a tumor where the immune system can exert some tumor control. We specifically looked at the players in the innate immune system, we found that RCC is a good candidate that could benefit from monotherapy. Our 1st step here is to test monotherapy AFM24. We believe that several important pieces are in place in RCC that an innate cell engager could work as a monotherapy. Of course, if we should see good data, that would not preclude that at some point we may add a combination with an NK cell or a PD-1. Again, for the first evaluation, RCC looks as one of those tumors where monotherapy could be quite beneficial for these patients. Okay, great. Maybe the last question, which is a housekeeping one, that in the second quarter of this year, the R&D expenditure as well as revenue has increased. Particularly R&D expenditure increased quite significantly compared to the prior quarter. For modeling purposes, should we anticipate the second quarter R&D expenditure will be something more as a base going forward for at least the remaining of the year? Yep. Thanks, Yale. A couple of comments there. One, we haven't provided specific guidance on our expenses, but we have provided guidance on our cash runway. What we've said is that we expect our existing cash, which is about a little over EUR 220 million, will last us into the second half of 2023. If you do the math on that, again, that's kind of eight to ten quarters out. That implies a cash burn in the low to mid-20s, excluding any impact of additional proceeds from loans or milestones, et cetera. Just based on that math, you can assume that the expenditure levels that you're seeing in Q2 of this year is probably more relevant as we go forward than the expenses you've seen in previous quarters, in particular, the second quarter of last year. Having said that, we do expect that R&D expense will be lumpy, right? This quarter, as I said on the call, we had an increase in AFM24. A lot of that's associated with production of clinical trial material for our ongoing study and upcoming studies. We've also had ramp-ups in our earlier-stage programs like AFM28 and AFM32. When it comes to CMC investments, those can be a little bit lumpy. Long story short, fair to assume that the R&D expenditure this quarter is probably more in line with where we'll be in the future than where we've been in the past. Okay, great. Thanks a lot. Again, congrats for a lot of progress here. Thank you. We have a follow-up question from the line of Nick Abbott with Wells Fargo. Great. Thanks for taking the follow-up. Just going back to the AFM24 trial, I believe that currently the trial's being conducted at 4 sites in the U.S., U.K., and Spain. Adi, you mentioned a U.S. CDMO. Can you talk maybe a little bit about, for the three expansion cohorts, how many sites that you expect to be running those trials at and whether they're going to be international or all in the U.S.? Will this be assignments or the two stage design for each of the cohorts? Thanks. Okay. Yeah. Thanks for this question, Nick. I'll have either Wolfgang or Andreas jump in here if they can. Yeah, I can. For the expansion cohorts of the monotherapy trial. We are looking to increase the number of sites from 4 that we are currently having, probably to somewhere between 10 and 15, 16 sites. Will continue to be a mixture of our U.S. site, international sites. You mentioned currently we have Europe. We will add a couple of sites in Southeast Asia, mainly Korea, especially to recruit EGFR mutant patients. The same is true for the PD-1, PD-L1 study, where we will have also a mixture of U.S. and ex-U.S. sites. Study 103, the SNK01 study, will initially be a U.S.-only study with up to 4 sites for the initial part and then expanding to a couple of more sites. Currently, the plans for this specific study are to be a U.S.-only study. In terms of the study design, all studies are designed according to Simon's two-stage principles. We will have an initial phase with a defined number of patients. Of course, as we are enrolling different disease types, the go/no-go criteria will vary by disease type. Also the definition of a response rate of interest will be a little bit different. In general, as I said, this will be Simon's two-stage designs with an initial cohort of probably around 12-15 patients, looking at a predefined success criteria, having the ability to enroll up to 30-35 patients per cohort, to verify the initial assumption of the Simon's two-stage design. Great. Terrific. Thank you very much. That concludes today's question and answer session. Ladies and gentlemen, thank you for participating in Affimed's second quarter 2021 financial results and corporate update conference call. This concludes the program and you may now disconnect.