Good day, and thank you for standing by. Welcome to the Affimed Financial Community Update Call. At this time, all participant lines are in listen-only mode. After the speaker's presentation, there will be a question and answer session. To ask a question at that time, you must be dialed into the phone line, and you'll press star, then one on your telephone keypad. Please be advised today's conference is being recorded. If you require operator assistance during the call, please press star then zero. I'd now like to hand the conference over to Alex Fudukidis, Head of Investor Relations at Affimed. Please go ahead. Thank you, Liz. I'd like to welcome and thank you all for joining us today to discuss the updated data from our investigator-sponsored clinical trial at MD Anderson Cancer Center. As you may remember, we released these data on November 22nd. Before we begin, I'd like to bring your attention to the fact that we issued a press release earlier today that includes updates to that data that will be discussed on the call today. This press release and a copy of today's presentation may be found on our website. Investors listening in on the webcast are also able to download the presentation from there. Before we start, I would like to 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 statements, even if the 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. Alex, thank you very much. I'd like to offer a warm welcome to all of you today, both our old friends as well as those who are newer to Affimed. I'm pleased you're here with us to further discuss the exciting data that we released just a few weeks ago. Before we dive into the R&D agenda, I first want to address what you are seeing in front of you. Yes, it's a new logo and a new color palette, but it's so much more than that. Over the past couple of years, we've evolved from being engineering and research-focused organization to a clinical development company with multiple assets in the clinic. We now have compelling clinical data from our lead assets validating our approach. Recognizing this, we thought it was the right time to evolve our visual identity in a way that more accurately reflects our passion and commitment to developing life-changing therapy. Yes, with that, let's move to the main purpose of the meeting. Joining me today from Affimed with prepared remarks will be Arndt Schottelius, our Chief Scientific Officer, and Andreas Harstrick, our Chief Medical Officer. In addition, I'm especially honored that we are also joined today by Dr. Yago Nieto from The University of Texas MD Anderson Cancer Center. Yago is an accomplished clinician and researcher with tremendous expertise in hematological oncology. All of us at Affimed are very impressed with his passion for his work, including his commitment to supporting his patients, which we've seen reflected in his ability to enroll so many patients in the trial with AFM13 and cord blood-derived natural killer cells. I'm excited for you to hear him present and share more of the data we previously screened. Moving to the agenda, I will start by giving a short refresher on our technology from which Affimed and our assets were constructed. Arndt will then continue to share relevant preclinical data that paved the way to starting the clinical study of AFM13 with cord blood-derived natural killer cells. Andreas will share insights on the clinical landscape around treating CD30-positive lymphomas to give you a frame as to where AFM13 combined with NK cells could potentially fit into the treatment paradigm. Now importantly, Dr. Yago Nieto will share a little more detail on the AFM13 patients treated to date. Of course, we will have time at the end to entertain your questions. Let me move on to show you what we have accomplished in the many years. At Affimed, we have positioned ourselves to be the leader in the activation of the innate immune system. As a clinical-stage oncology company, we understand the challenges with current IO therapies and recognize that many patients have been left behind. We're committed to developing novel therapies for patients who've exhausted other options, those who have failed multiple other lines. Our goal with Affimed is to broaden opportunities for activating patients' own immune system, innate and adaptive through monotherapy and, in particular, combination approaches. The biggest challenges we see with current IO therapies is that the potential of the innate immune system has largely been underestimated. Our goal at Affimed is to broaden opportunities for activating patients' own immune system, innate and adaptive, through the monotherapy and the combination approaches, of which the combination with NK cells could represent a game changer. We have shown that high efficacy is possible with natural killer cell-based approaches. The scientific premise around our approach is to address immune system evasion, in particular detection or recognition of tumor cells. Our technology indeed allows us to redirect innate cells, in particular NK cells and macrophages, to cancer cells and eliminate them. On the right, it is shown that indeed NK cell numbers matter, as cancer patients with larger numbers show usually a better treatment outcome. Our approach, as I explain further down, can address both the recognition of escaping tumor cells and providing a larger number of highly active natural killer cells. Indeed, our innate cell engager represents a very unique approach. They can bind to the immune cells with very high affinity, much higher than most other molecules out there. Indeed, that's an important fact. It is the basis to establish a tight bridge, indeed, between these immune cells and the cancer cell, which leads to immune cell activation and subsequently cancer cell destruction. Our innate cell engager represent a significant advancement over existing technologies, all are listed on the right side, and have been presented to numerous conferences. In total, in summary, this promises higher efficacy and better durability for patients that often have no further options. Now moving on to slide 11. We're indeed looking for different ways how we activate the innate immune system. First, we can do this with monotherapy. This allows us to activate just the two most important cells of the innate immune system, natural killer cells and macrophages. Thereby, we induce two mechanisms called ADCC and ADCP. This leads to tumor cell killing and, in an ideal case, also to the activation of the adaptive immune system, which then would cause a full immune response. We now far more fully understand the impact that the number of healthy NK cells have, especially for those patients who have failed multiple lines of therapy and are refractory to all other approaches. This is why we have evolved beyond monotherapy, and we're now developing our innate cell engagers in very specific combinations. That means that we have shown already, indeed with AFM13, that combinations with checkpoint inhibitors and NK cells appears to be very promising. Indeed, with natural killer cells, we're giving patients a new immune system, which means highly active NK cells, in our case, allogeneic NK cells, that have the promise to generate high response rates. This is what today's presentation will focus on. In summary, we have great confidence in our approach and the differentiated binding mechanisms to see this experience. We look forward to continuing to further develop our existing and future pipeline assets to improve the lives of patients living with cancer. This is also the moment to say thank you to all of the patients who have participated in this study. I will now turn over the conversation to Arndt. Thank you, Adi, and also from me, a warm welcome and good morning, everyone. In the next 10 minutes, I would like to lead you through our rationale for combining our ICE molecule, AFM13, with NK cells for the treatment of CD30-positive lymphomas. We know from clinical studies that the prevalence of NK cells and their ability to target tumors is associated with clinical responses. Naked and non-targeted NK cells, however, have limited persistence and only modest antitumor activity, which limits their broad use in cancer therapy. As we will show you, the combination of NK cells with ICE molecules may overcome these hurdles without the need for complex engineering or manufacturing. We are indeed exploring two distinct approaches in combining our ICE molecules with NK cells. We can either co-administer ICEs with NK cells, or they can be pre-complexed with our innate cell engagers. We can combine these innate cell engagers with NK cells. Common features of both of these approaches are that they are CD16A selective, that they lead to persistent arming of the NK cells, they result in enhanced tumor targeting and cytotoxicity, and both of these approaches are simple in their manufacturing. The co-administration can be done with either allogeneic or autologous NK cells. Important features of the pre-complexing approach are the opportunity for off-the-shelf NK cells, and that they can be easily expanded and activated, and may be particularly well-suited as an off-the-shelf option. Next, I would also like to summarize the key findings of our collaboration with the labs of Katy Rezvani at the MD Anderson Cancer Center, and Todd Fehniger at Washington University School of Medicine, which was recently published in Clinical Cancer Research. In this paper, we were able to show that AFM13 strongly binds to NK cells, inducing cytokine-activated or cord blood-derived NK cells, resulting in enhanced tumor recognition and ADCC. These exciting data form the basis for the successful IND of the ongoing phase I study with pre-complexed cord blood-derived NK cells at MD Anderson Cancer Center in patients with CD30- positive lymphomas, that we'll be hearing more shortly from our special guest, Dr. Yago Nieto, the principal investigator of the study. As you can see on the next slide on the left, the cytotoxic efficacy of pre-activated and expanded cord blood-derived NK cells, shown in green, is substantially enhanced by the combination with AFM13 over the cytotoxicity of only expanded cord blood NK cells, shown in light blue. On the right-hand side of the slide, you can see that the longer retention of NK cells after preloading these with AFM13 leads to a substantially higher degree of specific killing of CD30-positive tumor cells over a time period of 72 hours when compared to unloaded NK cells. This potent ability to kill tumor cells remains unaffected by washing the AFM13 preloaded NK cells. See the blue versus the red bars, demonstrating the ability of our ICE molecules to bind strongly and durably to CD16A on NK cells, and forming stable CAR-like complexes without the need for any substantial engineering. As presented just last month at the annual meeting of SITC, we have further characterized the mechanisms of action of our ICE molecules in a collaboration with Purine and Cells. On slide 17, you can see that the combination of AFM13 with NK cells greatly increases the cytotoxicity of these NK cells when compared to naked NK cells or AFM13 alone. This effect could be demonstrated with CD30- positive lymphoma and leukemia cell lines. As they say, a picture is worth a 1,000 words. You can clearly see on this next slide that we were able to demonstrate that the combination of AFM13 with NK cells significantly increased the proportion of NK cells that were killing more than three tumor cells. The ability of ICE molecules to thus render NK cells into serial killers is differentiated versus standard antibody technologies, and this, in our view, is contributing to the clinical efficacy we see in patients. Importantly, the highly encouraging preclinical therapeutic effects observed with AFM13 pre-complexed cord blood-derived NK cells, which we have licensed from MD Anderson Cancer Center, could also be reproduced when we pre-complexed AFM13 with peripheral blood mononuclear cell-derived NK cells. As you can easily see on slide 19, AFM13 pre-complexed PBMC-derived NK cells leads to near total abrogation of any tumor growth when compared to NK cells alone, AFM13 alone, or a non-targeting ICE control molecule. The striking in vivo data demonstrates the modularity in our approach of combining our ICE molecules with a different type of NK cells, leading to a strong therapeutic effect. At the upcoming annual meeting of ASH, we will be presenting data demonstrating the feasibility of cryopreservation and biological activity after thawing of pre-complexed NK cells with ICE molecules, which is important to establish the off-the-shelf utility of this approach. While I'm not able to share all of the details of the poster presentation still, as it is still under embargo, I can share that we have been able to demonstrate that the high efficacy of NK cells pre-complexed with ICE molecules is maintained after one freeze-thaw cycle, supporting this approach as an off-the-shelf method without the limitations and risks associated with CAR and NK cell technology. Now, in summary, I've shared with you that we at Affimed have preclinically assessed two distinct approaches in combining our ICE molecules with NK cells. For both of these approaches, we see great potential to overcome key hurdles known for naked NK cells. I've also shown you that the combination of AFM13 with NK cells forms stable complexes that exhibit increased cytotoxicity in vitro and in vivo. We have deeply characterized the mechanism of action of AFM13 in combination with NK cells, and we have demonstrated that cytotoxicity of NK cells and their ability to kill multiple tumor cells is greatly increased and clearly differentiated from standard technologies. Finally, as will be shown at the upcoming ASH conference, we were able to demonstrate that the high efficacy of AFM13 pre-complexed NK cells is maintained after a freeze-thaw cycle, supporting the fact that this approach could be developed as a novel cryopreserved off-the-shelf product. Now, with that, I will hand over to Andreas. Andreas? Yeah. Thank you, Arndt, and also from my side, welcome to everybody on the phone. Before we are going to discuss the study results, I would like to take a few minutes to review the landscape of CD30-positive lymphomas and to discuss the evolution of treatment strategies, specifically in Hodgkin lymphoma over the last five years, and what this evolution means for the treatment of patients with refractory Hodgkin's disease. Let's first turn to CD30 as a therapeutic target. In the design of AFM13, CD30 was selected based on two rationales. First, as you can see on the right side of the slide, CD30 is expressed on a variety of malignant lymphomas with very little expression on normal lymphoid tissue. Expression rates range from 100% in Hodgkin lymphoma to roughly 30%-60% in non-Hodgkin lymphoma, most notably peripheral T-cell lymphoma and diffuse large B-cell lymphomas. If you look at the incidence figures, each of these subtypes represents a quite interesting and valuable market opportunity. Adi will talk a little more about this in his final section. Second, and importantly, CD30 has been validated as a therapeutic target by success of brentuximab vedotin, even in very heavily pre-treated patients with CD30-positive lymphomas, indicating that the target is preserved on the malignant cell through multiple lines of therapy. This is also consistent with data that we obtained with AFM13, both as monotherapy and in combination, which show that patients can respond and do respond to AFM13 even if they have failed brentuximab vedotin. The target is preserved. Let's now move to the evolution of treatment standards in advanced Hodgkin lymphoma over the last couple of years. On slide 24, you see a treatment paradigm that existed probably like five, six years ago. First-line therapy, which is not on this slide here, always consists of a combination chemotherapy, usually using four to five different drugs like ABVD or BEACOPP. Now, for patients who did not achieve a complete response or who relapsed after a response, treatment alternatives were very limited. First salvage or second-line therapy usually consisted of combination chemotherapy. For a small subset of patients who were able to achieve another complete or near complete response, autologous stem cell transplantation. If you then move to second salvage or third line, treatment options were very limited. Basically another try of chemotherapy, which usually was palliative, radiotherapy to elevate symptoms. In very selected patients, allogeneic stem cell transplant, even palliative care was an established standard for patients with third- or fourth-line Hodgkin lymphoma. This landscape has changed over the last couple of years with two very important developments as shown on the next slide. These two developments were the introduction of brentuximab vedotin and PD-1 targeting antibodies into the treatment of Hodgkin lymphoma. As you can see in early trials in patients with chemotherapy refractory disease, most patients here had four to five lines of previous therapy. Objective response rates of around 70% were achievable, with roughly 20%-30% complete responses. Important to note, though, that especially brentuximab vedotin in these heavily pre-treated patients was also associated with quite significant side effects. More than 50% of patients here had grade 3 adverse events, and discontinuation due to adverse events was not uncommon. Even though these treatments, brentuximab vedotin and PD-1 targeting antibodies, were initially approved and introduced in refractory patients, late-line patients, they have not stayed in this position, as shown on the next slide. This slide reflects the current treatment paradigms or treatment guidelines for Hodgkin lymphoma. What you can see is that both brentuximab vedotin and PD-1 targeting antibodies, nivolumab and pembrolizumab, have nowadays moved to earlier lines of therapy. In case of brentuximab, it's used in first and/or second-line therapy. In case of PD-1 targeting antibodies, they are nowadays mostly used in second, third line. This evolution has two very important consequences. First, there is an increasing medical need for new therapy options in patients with Hodgkin lymphoma in third line and beyond. Because most of these patients will have been treated with brentuximab and PD-1 already in earlier lines of therapy, and thus are no longer available for third and beyond line treatments. Secondly, the patient populations that we are seeing now in our current studies are very different from the early brentuximab and PD-1 trials. As patients that we are seeing nowadays are not only refractory to chemotherapy, but they are also usually resistant to brentuximab and PD-1. Therefore, we cannot make any cross-trial comparisons with the early data generated with PD-1 or brentuximab. On the next slide is just a summary of what I just said. For patients who check basically all these three boxes, chemotherapy plus transplant refractory, BV refractory, PD-1 refractory, treatment options become increasingly limited. There is a significant need for new treatment for patients with relapsed and refractory Hodgkin lymphoma. Furthermore, as these heavily pre-treated patients have frequently impaired organ function, there's also a need for effective but also well-tolerated treatment options. There are two developments in these patients that are worthwhile to mention on the next slide. These are, camidanlumab tesirine, another ADC, and of course CD30 CAR T-cells. As you can see, both treatment paradigms or both treatment strategies have shown quite interesting early response rates. However, especially camidanlumab tesirine has also been associated with very significant side effects. Over 60% of patients have grade three toxicity, including liver function abnormalities and Guillain-Barré syndrome. There is a quite high discontinuation rate due to treatment emergent adverse events. As you know, CD30 CAR T-cells are also associated with toxicity and also a quite laborious manufacturing process. To finalize and to set the scene for the discussion of the study results, I hope I could show you that CD30 is a interesting target universally expressed in Hodgkin lymphoma and to varying degrees in other B and T cell lymphomas, making it an attractive target with a good market opportunity. The movement or the positioning of brentuximab and checkpoint inhibitors to earlier lines of treatment has clearly created a void and a need for new treatments, for patients with relapsed and refractory disease. Specifically for Hodgkin lymphoma, we are confronted with two different clinical situations. For patients who are transplant eligible, the goal of new treatment has to be to induce deep responses, near complete responses or complete responses as a pre-precondition for a transplant. Also for patients who are no longer transplant eligible, deep responses are needed to control tumor burden and tumor burden-associated symptoms. As I said, a special need here for these heavily pre-treated patients, not only for effective treatment, but for treatments with a good safety profile. With this scene setting, it's my pleasure to hand over to Dr. Yago Nieto, professor at MD Anderson Cancer Center and principal investigator of our study with AFM13 in combination with cord blood-derived NK cells. Yago, please. Thank you, Andreas, and good morning, everybody. It's my pleasure to present on behalf of my co-investigators at MD Anderson, the first preliminary results of our ongoing trial of innate cell engager, AFM13, combined with pre-activated and expanded cord blood-derived natural killer cells for the treatment of refractory CD30-positive Hodgkin and non-Hodgkin lymphomas. Next slide, please. This study is testing for the first time in patients the novel approach of combined adoptive cellular immunotherapy conjugated to a bispecific innate cell engager. The underlying biological principle is that pre-complexing the NK cells with a bispecific engager AFM13, which has affinity for both the natural killer cells and for the Hodgkin lymphoma cells, markedly increases the cytotoxic capacity of the NK cells. Next slide, please. Can I have the next slide? Slide number 35, please. In a series of carefully conducted preclinical experiments, Dr. Katy Rezvani, my co-investigator, and her lab team observed that pre-complexing NK cells with AFM13 prior to infusion facilitated CAR-like responses by NK cells. Based on technology she previously created, persistence of NK cells could be enhanced by pre-activating those cells with a cocktail of cytokines including IL-12, IL-15, and IL-18 to induce a memory phenotype of the NK cells. As you can see on the right side panel, mice with tumor xenografts of Karpas, and Karpas is a lymphoma cell line that is intrinsically resistant to NK cells. Mice showed superior outcomes when treated with pre-activated and expanded NK cells that were derived from cord blood and loaded with AFM13, as compared to mice treated with the same pre-activated and expanded NK cells but unloaded with AFM13 or to mice treated with AFM13 alone. Next slide, please. Those very exciting preclinical results led us to test in the clinic the hypothesis that we can infuse ex vivo expanded cytokine-induced memory-like cord blood-derived functional NK cells whose specificity is redirected against CD30-positive tumors, but by pre-loading those cells with AFM13 prior to the infusion. The advantages of using off-the-shelf... I'm sorry. Yeah, that's the right slide. Thank you. The advantages of using allogeneic, off-the-shelf umbilical cord blood-derived NK cells is that they're number one, they're readily available. We can get them from any of the cord blood banks. They can easily be expanded to a larger scale around a thousandfold in 14 days. This is following a technology created by Katy Rezvani and Dr. Elizabeth J. Shpall, who are co-investigators in this trial. Importantly, we have shown, excuse me. Can we go back to the previous slide, please? We have shown feasibility and safety in clinical trials in myeloma and non-Hodgkin lymphoma, where more than 100 patients at MD Anderson have been treated with no toxicity and promising clinical activity. This is completely consistent with the biology of NK cells, which are hardwired to not react against normal cells. Next slide, please. This is the treatment schema. Cord blood-derived NK cells are manufactured over two weeks in our GMP lab, during which time they are pre-activated with cytokines IL-12, IL-15, and IL-18 and expanded with universal antigen-presenting cells. At the end, they're incubated during one hour with AFM13. In parallel, at the end of those two weeks, patients receive lymphodepleting chemotherapy with fludarabine and cyclophosphamide. Now, these drugs are not expected to treat the lymphoma, but rather to suppress the patient's own immune system and therefore increase the persistence of the cord blood NK cells. Two days after the end of the chemotherapy, patients are infused with the AFM13-loaded NK cells, and subsequently, once a week, they receive three intravenous doses of AFM13 alone. This is based on our preclinical work, where we saw that the half-life of AFM13 on the surface of NK cells is around a week. All of this constitutes one cycle of treatment, and patients receive two cycles. The whole trial is a phase I trial where we have escalated the dose of NK cells per cycle from 1 × 10^6 per kilo to 1 × 10^8 per kilo. On the next slide are shown the trial's eligibility criteria and basically they require adequate end-organ function, but patients don't necessarily have to be in outstanding shape. In fact, many of them were not. Also, please note, as shown in red, that all patients require to be refractory or intolerant to brentuximab vedotin, which is the drug, the approved drug that also targets CD30. This is the common target with AFM13 on the surface of the cells. On the next slide, you can see the study endpoints. Primary endpoint being a phase I trial is to establish the safety and the recommended phase II dose of the cord blood NK cells. Secondary endpoints are to assess the overall response rate, including complete and partial responses, to evaluate the overall survival time, to quantify the persistence of infused donor cord blood AFM13 NK cells in the recipient, and to conduct comprehensive immune reconstitution studies. Now, the study is still ongoing, and we have firm data on the safety and recommended phase II dose. We have data, ongoing data on activity and we don't have data yet on overall survival or the correlated studies. Next slide, please. This is the patient population enrolled to date. The age, gender is what you would expect in a group largely composed of Hodgkin lymphoma. There were also two patients with CD30-positive T non-Hodgkin lymphoma. Of course, all patients have received prior brentuximab vedotin, and the vast majority of them have received an anti-PD-1. Most of them have received a previous autologous transplant. There were two patients who had previously failed CAR T. Importantly, this was a very heavily pre-treated population with six prior lines of therapy, five prior episodes of relapses of progressive disease, and all 19 patients had progressive disease to the immediately prior therapy. In other words, their tumor was growing coming into treatment. Next slide, please. The treatment was shown to be very safe. There were no cases of cytokine release syndrome, neurotoxicity or graft-versus-host disease. There were only five cases of infusion-related reactions in 108 infusions of AFM13 alone for a very low infusion reaction rate. No dose-limiting toxicity was encountered, and dose level 3 at 10^8 NK cells per kilo was established as the recommended phase II dose. Next slide, please. This slide shows the antitumor activity. We saw responses in 17 of the 19 patients for an overall response rate of 89.5% with seven complete responses and 10 partial responses. Importantly, all 13 patients treated at the recommended phase II dose responded to cycle one. Responses to cycle two are still being evaluated, and there were five complete responses and eight partial remissions. Now, on the next slide, I want to illustrate the quality of these responses with a couple of patients enrolled in the study. The first case is a 44-year-old male with a long history of Hodgkin lymphoma, which was diagnosed back in 2014. This patient failed several lines of therapy, including ABVD with a primary progression to it, followed by bendamustine brentuximab, which is a highly active first-line salvage regimen to which it didn't respond either, third line with ICE produced a brief complete response which served to take him to high-dose chemotherapy and autologous transplant, but the patient subsequently relapsed. He then received several lines of salvage, including pembrolizumab, camidanlumab tesirine, which is a new antibody-drug conjugate Andreas referred to which he had a complete response followed rapidly by a relapse. Finally, and right prior to study enrollment, he received nivolumab with progression, a progressive disease. He was enrolled on the trial and treated at dose level 3 with no side effects. On the next slide, you can see the complete response he experienced on his left side bulky cervical lymphadenopathy. This lymphadenopathy you could actually see it from the door. It was huge. He had a complete response to it after cycle 1. He received cycle 2, and he remains in unmaintained CR at more than six months. The next case is a 31-year-old patient from Abu Dhabi in UAE who was diagnosed with Hodgkin lymphoma in 2005. He received the German regimen BEACOPP as first line with a complete response. Following the first relapse, he received salvage with ICE, followed by high-dose chemotherapy and autologous stem cell transplant, had a second relapse, received GVD with a complete response. The patient declined at that time an allogeneic stem cell transplant, and that was a missed opportunity as we could see, because over the following years, he relapsed and received multiple lines of therapy to which he experienced short-lived responses at best. Those lines of therapy, as you can see here, were brentuximab, Nivo, Doxil and lenalidomide, ibrutinib, and gemcitabine, bendamustine and Navelbine with a complete response which was enough for his local doctor to refer him to Johns Hopkins for an allogeneic transplant. When he was seen there, he was found to be in widespread progression with new large lesions in the liver, several of them around three centimeters each, spleen, retroperitoneum, peripheral lymph nodes, bones, and bone marrow. He had tumor, essentially, he had tumor everywhere. Our colleagues at Johns Hopkins referred him to us to MD Anderson for this trial. He was treated at dose level 3 with no side effects. As you can see on the next slide, after cycle 1, multiple sites of disease, both nodal and extranodal, including liver and bones, experienced a very gratifying complete response. The patient received a subsequent cycle 2 with the same results of complete response, and he remains in CR at three months. Next slide, please. This leads us to the important topic of durational responses. In the first nine patients, of whom seven had a response, as you can see here on this column on the left, with five CRs and two PRs, there were three patients at recommended phase II who have ongoing responses at more than six months. One of them is currently receiving maintenance pembrolizumab. The other two are unmaintained. Of note, the first patient who had a PR, this was consolidated with an autologous transplant, 5.5 months following study treatment. Next slide, please. In conclusion, this is the first clinical trial using an ICE construct pre-complexed with off-the-shelf ex vivo expanded cytokine-induced memory-like cord blood-derived NK cells to treat patients with CD30-positive relapsed or refractory Hodgkin's and non-Hodgkin's lymphoma. Our preliminary results indicate that this novel cell therapy has an excellent tolerability profile and is highly active in patients with heavily pretreated refractory or relapsed CD30- positive lymphomas, and this approach warrants further investigation. Lastly, Next slide, please. I wanna thank all the co-investigators in the study, both from the lab and the clinical side, as well as our friends at Affimed who are sponsoring this study. Without further ado, I will hand the call back to Adi. Thank you very much for your attention. Yago, this was great. Thanks a lot. Indeed, as I think back to earlier conversations with your colleague at MD Anderson about creating the preclinical work, I think I cannot help but stand here today and reflect upon what we've accomplished. Since those first days, milestones are very remarkable. The data you shared with us today is exciting and creates a promising outlook for patients who might otherwise have no options. Indeed, there is potential in the unmet need in the marketplace for such a therapy. What we have done is we have conducted a market research study in order to better define the opportunity for AFM13 within the treatment. We've been told by patients, and we've confirmed that there's a high need for a novel therapy, both in Hodgkin lymphoma and other subtypes of lymphoma, including T-cell lymphoma, but also there's definitely hope for a novel mechanism as physicians look for pathways that have remained unexplored, specifically the role of NK cells, as we've just seen in the fight against cancer. Indeed, payers see this approach as a novel armed and directed cellular therapy that has a substantially better safety profile than that of CAR T. Now, the avoidance of eventually paying for the high cost of delivering CAR T, as well as the associated complications, have basic payers leaning towards using CAR T therapy as the analog for pricing, which we believe is enriching from a commercial point of view in an indication where we, as we have shown, have a real number of patients. As we have learned, CD30 is a validated target, indeed in a wide range of lymphoma indications. Andreas discussed that before, and there are patients either with Hodgkin lymphoma, diffuse large B-cell lymphoma, peripheral T-cell lymphoma, and cutaneous T-cell lymphoma with various degrees of CD30 expression. Some of them indeed only have very few lines of therapy and need much better treatment. By 2013, combined with metric, the cell indeed holds the promise to allow patients to have more time with their families and make more memories. Every patient matters to potential price analogs. The combination represents a very attractive opportunity. Our goal is to be able to address most of these patients in the relapsed refractory setting, initially, which in and of itself is attractive with a potential addressable patient population of about 5,000 patients just in the U.S. I believe, given the safety and efficacy that proved up in the treatment paradigm, which would represent a significant expansion opportunity. While these numbers represent the U.S., we believe there is also a similar opportunity in Europe and in other regions. We're now committed, as we see on the next slide, in order to move forward with it. There were a number of accomplishments. Now let me talk about AFM13 in all its clinical studies. If you might recall earlier this year, we did report on the preplanned interim analysis of our registration-directed study of AFM13 monotherapy for a 12-week follow-up. Based on the interim analysis, we're going to continue the study combining the high and low CD30 expression form. This was a novel finding in that we saw comparable efficacy in the high and low expressors. It demonstrates the strength of our technology that we can achieve efficacy independent of target expression. Moving to the combination here at the AACR, Dr. Katy Rezvani shared unexpected and impressive data from the first four patients treated with this combination of cord blood-derived NK cells with AFM13 at the lower doses. Again, I'd like to thank the patients and our partners at MD Anderson. Where do we go from here? In 2020 and beyond, we want to build on this momentum and find a path to bring AFM13 as monotherapy and in combination with NK cells to the market. We will do this by completing patient enrollment in the registration-directed study of AFM13 in peripheral T-cell lymphoma. We're maintaining our guidance to complete enrollment in the first half of 2022. We're further treating patients with the NK cell combination. The protocol amendment was submitted with the aim for 40 patients with relapsed/refractory PTCL as the recommended phase II dose. We look forward to updating you at medical conferences as the study proceeds. We're also planning a meeting to consult with the FDA on how to support a registration-directed study for AFM13 in combination with rituximab. Now, taken together, we believe that AFM13, based on its safety and efficacy, addresses patients with very limited options, and it appears to represent a significant commercial opportunity. We are applying our learning indeed, and successes to our growth platform. When we look at the next slide, you can see two molecules listed, AFM24 and AFM28. As we reported, on the right side, we have created an additional opportunity for patients with adult leukemia. Now, why CD123? It is expressed on both leukemic blast and stem cells, and represents an opportunity to address relapse that still occur in far too many patients. Really, we are excited about the opportunity for this targeted natural engager molecule as outcomes in AML remain dismal. Preclinical characterization will be showcased at ASH, and we are very excited now to move this molecule forward into the clinic, and we believe that we can start clinical studies in the second half of next year. This brings me to the milestones. As we've shared previously, our next step for AFM13 is to conclude the enrollment of patients with CD30- positive peripheral T-cell lymphoma, originally recruited into two different cohorts that are different by CD30 expression, and we expect to complete the enrollment in the first half of 2022. With AFM13 in combination with NK cells, we have completed the dose escalation, and as I just mentioned, we have submitted a protocol amendment that will allow us to treat four more patients, giving us multiple opportunities now to present additional data at upcoming medical conferences. We're quite honored to work together on this, on these presentations with Yago Nieto, Katy Rezvani, and additional investigators. For AFM24, we have met a very important milestone that we could determine the recommended phase II dose, not just to be safe, which is already differentiating from other EGFR-targeting antibodies, but it was pharmacologically and pharmacodynamically active. This allowed us to initiate the dose cohort expansion into select indications, where we have analyzed that these indications have a high chance for innate immune cell activation. We believe that we can provide multiple updates in 2022. There are these two combination studies, and, as we've just announced yesterday, we are now recruiting patients into the study, into the combination study with the anti-PD-L1 antibody, and the NK cell combination study already has been reported to be recruiting. Two very exciting studies. Again, unique approaches and many people are trying to combine NK cells with EGFR-targeting antibodies. Again, as we've shown throughout this presentation, the differentiation is the affinity and the specificity towards CD16A, which we believe can have a much more profound effect. I'm again mentioning AFM28 here on just given the block, on the block. Pre-clinical data would present it in a week from now, just in a couple of days. IND filing is planned for the first half of next year. We are in a quite intense preparation of a clinical study that definitely will be a monotherapy study. We're also looking forward to bringing AFM24 forward in a combination study with natural killer cells. On our partnerships, we continue to make very good progress. Indeed, with a number of molecules, we have them now in pre-clinical development and hence they are advancing to IND filings. As we've said, this could bring in additional milestones. On the other side, just for us, we have a number of novel targets identified. We have picked these targets and started the generation of novel innate cell engagers. We can either use them to broaden our pipeline further, or we can take these molecules into forming additional partnerships. All this progress and outlook supported by a strong help of our investors. Indeed, as we've mentioned in the past, we have a good cash position that takes us into at least the second half of 2023. With this, I would like to thank again my speakers in particular, all the speakers, in particular my colleagues and Dr. Yago Nieto for their presentation. I will now open the call for questions, and we'll provide the answers. Thank you very much. As a reminder, to participate in the question-and-answer session, you must be dialed into the phone conference. If you'd like to ask a question at this time, please press the star, then the number one key on your touchtone telephone. To withdraw your question, press the pound key. Our first question comes from Kripa Devarakonda with Truist Securities. Hey, guys. Thank you so much for taking my question and congrats on all the progress. One question I have is almost everyone in this trial is responding to the treatment, but the initial dosing seems to correlate with durability. Is that a fair statement to make? And then in addition to dose, the dosing, do you see any other metrics that correlates to durability? And then you talked about discussing with the FDA about moving into registration-enabling trials next year. Can you talk about what the gating factors for those are? Would you need to see additional data from this, especially from the second dose in these patients, and anything else that you might need to take to the FDA to discuss potential registrational thoughts? Thank you so much. Kripa, thank you very much. I'll hand these questions over to Andreas, who may discuss what's required in order to get to FDA, and then Andreas will hand it over to Yago to give the answers on your clinical questions. Andreas? Yeah. Thank you. So excellent questions. I think for our FDA interactions, from the clinical point of view, I think we have a pretty good database. Of course, we would love to have a little bit longer follow-up on the additional patients who are treated at the recommended phase II dose level. In parallel, as we have announced, we are also working on establishing a manufacturing process, a stable manufacturing process that would enable multi-center trials and registration trials. This is the other piece of work that is going on in parallel, and I think once we have those, a little bit longer follow-up with the patients at the recommended phase II dose, as well as, iron out some of the production issues that we still have to work on, this would be a good time to go to FDA for consolidation. In terms of the dose effect on response quality and response duration, I think I will hand over to Yago, who has seen most of, basically all of these patients, to take that question. The durability in our preliminary data does appear to be a dose response effect. This is with the caveat that the study is ongoing. It does confirm though the observations we previously made in our lab, where higher doses of NK cells resulted in longer responses in tumor xenograft in mice. This data is still ongoing, the clinical data, I mean. Great. If I can ask a follow-up question. What was the rationale for one of the patients that was in the highest dose to go on to PD-1 therapy? Because you mentioned that I think the PR mentioned that two of the three patients continued their CR six months and beyond without any additional therapy. Can you maybe provide a little color on what made you decide to put the patient on the PD-1? Thank you so much. Yes, I can. That patient, in fact, is a patient of mine. It's a young woman with a very high-risk Hodgkin lymphoma, multiple previous relapses, early progression after a previous autologous stem cell transplant. The reason why I started maintenance anti-PD-1 was after discussion with the patient. After achieving the complete response, I discussed with her doing allogeneic stem cell transplant, but unfortunately, it has not been financially cleared yet by the third-party insurance company. In the meantime, and given that anti-PD-1 might be, it's a, you know, well-tolerated, I decided to start some maintenance treatment, knowing that she's already in CR. Great. Thank you so much. That, that's excellent color. Thank you, doctor. Thank you. Our next question comes from Daina Graybosch with SVB Leerink. Hi. Two questions from me. The first I think follows the last one, which is, I believe, and can you confirm, this is a two-cycle treatment. If patients aren't going to transplant, how are you thinking about broader longer-term maintenance if it's necessary? Would you ever use three cycles, use another cycle if patient starts to progress, continue the AFM-13, maintain with pembro? I think there's a lot of options here, and I'd really like to know how you guys are thinking about it both MD Anderson and Affimed. My second question is also on the durability. You have some of these patients, you know, time from study to relapse or subsequent therapy. I believe some of them went on to transplant, and I wonder if you could confirm which of these patients went on to transplant or a different therapy. Thank you. That's an excellent question. Right now, the way we designed the protocol was to allow for two cycles. Of course, that was before we knew how well tolerated and how safe this treatment is. The FDA just approved an amendment that will allow us to give more than two cycles. Strategically, when we have a patient who is transplant eligible, I think two cycles offers that patient an excellent chance of achieving a complete response, which could serve as a unique opportunity to take the patient to transplant. Alternatively, you know, given that the treatment is so well tolerated, we can give more than two cycles. You know, we are potentially looking at up to six cycles, same as the number of cycles one gives for adjuvant chemotherapy for pretty much every single human tumor. This is, you know, speaks of the two different opportunities for patients who are transplant eligible and those who are transplant ineligible. It gives us a lot of flexibility for both types of patients. Yeah, I think nothing to add here. I think what we have seen, and Yago confirmed, is an excellent tolerability of this treatment, even with this very heavily pre-treated patients. There's always the option to give more cycles, and then we believe that, especially in patients who are not transplant candidates, this will result in a long-lasting tumor control. Now coming back to the question for transplant patients, again, as Yago said, patient who achieves a CR probably has optimal induction with two cycles. You may argue whether you want to give a third cycle, but that's probably the window where you would consider a consolidated transplant. In fact, I think, Yago, we have one patient who received a transplant out of the nine patients that were on the dose escalation parts. This is patient one, received transplant 5.5 months after starting NK cell-based therapy. As far as I know, but Yago please confirm, this patient is still in complete response, and he's now far over a year after starting the whole treatment sequence. Yes, that is correct. Are there any others that receive transplant, I guess, of these other three patients 2-4? Of those nine, the only one who received a transplant is the one we were just discussing. There are a few of the patients enrolled at the dose level 3, the recommended phase II dose, who are transplant eligible, and we are looking at their complete responses as a unique window of opportunity to proceed with transplant. Though many of those patients are folks who had never responded to anything before, and their referring physicians were desperately trying to induce a remission that could take them to transplant. That's a different, like we said, it's a different population from those who are not transplant eligible, and where it looks like the best strategy might be to give more cycles of AFM NK cells. Got it. One follow-up, after the six cycles, because the cycle has chemo and then the combination, do you think there would be any benefit for continuing the AFM13 alone? There might be. Yes, there might be. Great. Thank you very much. You're welcome. Our next question comes from Maury Raycroft with Jefferies. Hi. Good morning. Congrats on the progress, and thanks for taking my questions. I was wondering for the secondary endpoint on cord blood NK cells plus AFM13 complexes and the persistence of those, can you comment on what you're seeing so far, and if you'll provide data on that in your first half 2022 update? That data is still being analyzed. We do know that NK cells, the cord NK cells persist for up to three weeks, but we don't have any firm data yet. Hence the rationale for more than one cycle. We hope that we will provide with this very important persistent data in our next update. Got it. Okay. I believe the data so far is with using the fresh complex of cells plus AFM13. I'm wondering when you plan on switching to using the freeze-thaw complex product. You mean, frozen NK cells? Yeah. Correct. We're working on that. You know, NK cells are not easy to freeze, and we're working on that. We are making significant progress, and we hope that it will be realized in the near future. Yeah, that would definitely provide with a truly off-the-shelf cell product. You're absolutely right. Great question. Okay. Last question could be premature on this, but just wondering if you could talk more about what different scenarios could be on outcomes from the registration path conversations with FDA on the AFM-13 plus cord blood cell combo studies in 2022. Andreas, you want to take that? Oh, yeah, I think. Yeah, yeah. I think it's a little bit premature question, because we definitely have to talk to FDA. Now, looking at the data, again, response rate I think is highly impressive. When we started out, we thought that 50% would be great. Now we are at 100%. I think especially with the recommended phase II dose, that's outstanding with these heavily pre-treated patients. So we have the firm belief that there should be an opportunity for an accelerated approval process based on the phase II study. I think that will be details we have to discuss with FDA, what's the right patient number, what's the inclusion criteria defining a patient who is refractory. I believe this is a treatment that needs to get to the market and needs to be available to patients as soon as possible. This is really game changing. I would be very surprised if FDA would see it differently. Our assumption is that we will have the opportunity to go for an accelerated approval. Very good. Shall we move to the next step? Our next question comes from Brad Canino with Stifel. Hi, thanks for the details and congrats on all the positive progress with this trial this morning. I guess one more on subsequent therapies for me, which it sounds like the investigators have used preemptively here rather than in response to any loss of depth of response. In the 12 RP2D patients that just finished the second cycle, how many might you expect to have a transplant or PD-1 maintenance? Is it 2-3, half or maybe more? At this point, given that we just got the amendment to allow for more than two cycles just approved by the FDA, we have all remaining patients lined up for some subsequent therapies. In most cases, it will be a transplant. Lot of those patients had already failed an autologous transplant, so we are looking at an allogeneic transplant to take advantage of their CRs. In the future, this may change as we have more of the opportunity to give more cycles and we may see how durable sequential cycles more than two without consideration for transplant might be. But the remaining patients at the RP2D dose are largely lined up for transplant, yes. Okay. For the Affimed team, maybe when might we see the next update here? Because, you know, at the low doses you largely had these relapses less than six months, but the three high dose in the dose escalation had durability beyond six months. At the next update, what's your rough estimate for how long the RP2D patient cohort will be in duration terms? Because I'm wondering if that could serve as a confirmation of this dose response on durability based on when you're planning to release more interim data. Andreas, do you wanna go for this? Yes. We, I think said earlier today, we are collecting the data with the additional patients, and our goal is to target a significant scientific conference in 2022 to release the totality of this data. Okay. Well, I look forward to update. Thank you so much. Our next question comes from Nick Abbott with Wells Fargo. Good morning. Thanks for taking my questions. Yes, congratulations on the data and the spiffy new look. I like it. First question really is to Dr. Nieto. Can you talk about, you know, depth of complete response? I've been doing this long enough that many of these diseases, you know, complete responses were rather rare, and if you got one, people didn't really question about how stringent those responses are. Now we have MRD, so how do you think about CR depth? Is there an MRD assessment? I guess, you know, that's leading to how do you know if a transplant is going to increase that depth of CR to cure? That is a great question. As you know, the ultimate test to evaluate response right now in Hodgkin lymphoma is a PET scan. We, as well as many other groups, are working on molecular techniques to determine and measure cell-free tumor DNA in serum, which is a great assay in B-cell and Hodgkin lymphoma, but still in progress in Hodgkin lymphoma. We're working on that, and it would be critical to segregate those patients in CR into those with MRD negative responses in serum versus those who still have detectable tumor DNA or MRD positive. That is crucial. As far as your next question as to whether transplant can increase the depth of the responses we see with this therapy. Well, it goes again back to the all-important issue of cell-free tumor DNA. Based on 30 years' worth of clinical research and experience, transplant is curative in relapsed Hodgkin's, particularly if they are in CR at the time of transplant. In that sense, only time will tell. If we have a patient who we have transplanted and remains in remission two years after transplant, chances are very high that that patient is already cured based on all our, you know, prior clinical experience. It will be highly instrumental to be able to use MRD tests the same way we do in leukemias or in multiple myeloma or increasingly in diffuse large B-cell lymphoma. Great. Thank you. The next question is on, you know, what are your thoughts about moving to earlier line patients, first relapse, for example. What are the barriers to doing, you know, at least a small trial of, you know, frontline ABVD plus minus these pre-complex NK cells? That is a terrific question. Of course, you know, it's strategically from a clinical standpoint, once this therapy is FDA approved, one of the routes of progress would be to move it to earlier lines of therapy, given its very favorable safety profile compared to pretty much any other chemotherapy for treatment for Hodgkin's, including non-chemotherapy options. Absolutely. It's, you know, using it early on in relapsed patients or ultimately even in frontline is something that should warrant investigation. Thank you. Last one from me is, you know, I'm interested, you say you now have got approval to do up to six cycles. You know, I think, generally what we hear is that, you know, the lymphodepletion regimen is often seen as a barrier. You know, we've heard other companies say, "Well, you know, maybe a couple of cycles of Cy/Flu, but beyond that is pushing it." It seems like you have a different opinion here that, you know, patients will tolerate, even these very advanced patients will tolerate multiple cycles of. Yeah. Yeah. -Cyflu. Thank you. I probably have a different opinion. You know, if you think of a different scenario, different setting, which is chronic lymphocytic leukemia. You know, a well-established and time-honored regimen for those folks is FCR, which is essentially fludarabine cyclophosphamide, which is the same lymphodepleting chemo we use with our cycles of AFM and N K plus rituximab, right? You know, you can give FCR for six cycles to patients with CLL who are, you know, for the most part they are older, and they don't have much marrow reserve without much problem. I don't see. I mean, it could be my toxicity could be limiting in the occasional patient, but in general, I don't see that. I don't envision that as a limiting factor in this patient population. FluCy is lymphodepleting, but it's not very myelotoxic. We see a drop of the white cells transient for a few days, and they recover rapidly. I don't think that would be ultimately limiting this strategy. Terrific. Thank you very much. You're welcome. Our next question comes from Yale Jen with Laidlaw & Company. Good morning, and thanks for taking questions, and my congratulations as well. My first question here is that, from the physician's or from company's perspective, what might be the hurdle rates for a third line, in Hodgkin lymphoma, both in terms of response rate as well as in terms of duration of response, as well as other sort of metrics? Andreas, can you take that question, please? Yeah, I think again, it's a difficult question because we only know what FDA thinks once we have talked to FDA. If we look across other lymphomas and then also, after talking to those physicians and payers, we would believe that everything around 50% or above 50% in terms of response rate and duration of responses in the six months area would be a very meaningful advantage and probably constitute a reasonable estimate of where we should be. Okay, great. That's very helpful, and certainly you guys have a seat at the moment. My second question is that we certainly understand the patients still expressing CD30 as the drug treatment are effective at this point. I'm just curious, in terms of patients refractory to multiple treatments, what level of CD30 expression levels still they have? Yeah, I can answer that. Interesting factor about Hodgkin lymphoma is that even after extensive prior brentuximab treatment, patients, once they fail it, they still express CD30. I think that I can only recall one patient out of many who we have seen for this trial, and we have lined up who was CD30 negative after a lot of prior brentuximab. In that regard, that's not a big problem. On the flip side, once the patients who have relapsed after AFM13, they do still present CD30- positive on the surface. Oh. Okay. Maybe my last question here is sort of generally about the NK cell combinations, which is that it seems that this allogeneic system works very well at this point. Would that be a possibility that going forward, eventually all the NK cell combinations or, you know, co-administration will be from allogeneic instead of autologous? Or you feel the autologous still have its value in a different context and effects? In the current trial, I guess to deal with the Hodgkin lymphoma and NK cells, this is an allogeneic trial. No matching has been done. You probably are referring to the study that's now recruiting, where we combine AFM24 with autologous cells, that's treating solid tumors. As I said, we're focusing on lung cancers, colon cancers, and head and neck cancers. Here we have chosen this. We were thinking as a quick step into the clinic, to work with this autologous. I think you know NK cell. We aim to establish a proof of concept with this approach. Obviously it depends on data we decide on next steps. For us, and not only for us, but also for others, we plan to pursue the combination with allogeneic cells in solid tumors. Certain regimens, certain preparations are not yet established in solid tumors, so that's why the autologous approach can have initially some advantage of we don't have to lymphodeplete patients. The autologous cells can be infused on a weekly basis and are maintained in the patients. Even when we dose these patients later than three, four, five, six weeks, the NK cell infusions basically are increasing the numbers of NK cells in these patients, which then are redirected by AFM13 to attack the tumor cells. You have simply the opportunity to treat much longer without lymphodepletion. There is also some advantages. We see that the allogeneic approach can be turned into a full off-the-shelf approach, and that obviously would make this much more convenient for getting access to such drugs. You see that each of these approaches at the moment not only warrants an investigation, also obviously some very big implications if you can generate responses in any of the patients as they will very severely sick. Okay, great. Thanks. Again, congrats. Thank you. Our next question comes from Zhiqiang Shu with Berenberg. Hi. Thanks for taking my question, and congrats on the data as well. First question I wanna ask about the two patients in the middle dose that did not respond. I guess for the doctor and the company, can you provide any color around what the kinda characteristics of these two patients? They were heavily pretreated as pretty much every other patient in the trial. They received the middle dose level, which is one log less than the recommended phase II dose. They experienced progressive disease after treatment. Not much more to comment on them. The treatment was fortunately very well tolerated. At least it didn't have any toxicity, but they didn't respond. Okay. Great. Thank you. The second question I wanna ask is about the kind of the quality of the CRs. Obviously, if you look at the CRs in the lower dose, they seem to have a shorter duration response as compared to the CRs, three CRs that you that deal with the recommended phase II dose, which seems to have longer than six months duration response. I guess, Doctor, from your perspective, what differentiates those CRs? Yeah. This, like I said, this is data that's still ongoing. We're still enrolling more patients. The data, there does appear to us that there's a dose response effect that reflects on the durability of responses and also on the likelihood of achieving a complete response. In terms of other features of the CRs depth, some of the PET scans, some of which I showed, they're really impressive. We are working in parallel to the trial into trying to determine at a molecular level the depths of those responses, but that is still experimental at this point. We're hoping that with more patients, we'll have more data as to how the dose of NK cells translate into more durable responses. Got it. I think this is quite important because as you alluded earlier, you have modified the protocol to allow for six cycles of treatment. So if the CRs are different, I guess the question is when should you continue treatment versus stop the treatment between two to six cycles? What’s your thought around that? Right. That is a very important question. So you have to determine whether a patient is transplant-eligible or ineligible. If you have a transplant-eligible patient, I think once you achieve a complete response, you can start considering this patient for transplantation, preferably autologous, if the patient has not received it yet. And perhaps given an additional cycle to buy time while we secure financial approval for the transplant and get the patient ready. Patients who are, on the other hand, transplant-ineligible, I think will clearly benefit from a more prolonged course of treatment, more cycles. Got it. My last question is around two non-Hodgkin lymphoma patients that were enrolled in the trial. Can you provide their characteristics and their response in the trial? Then for the company, how should we think about the potential opportunity in the CD30- positive non-Hodgkin lymphoma patient? Those two non-Hodgkin lymphoma patients, they had a T-cell lymphoma expressing CD30, and they were both very heavily pretreated. One of them was treated at dose level 2, and it was one of the patients who did not respond. The other one was treated at dose level 3, the recommended phase II dose, and he has achieved a partial response, which is almost. It's technically a partial response. If you look at the PET scan, it's practically a CR. That is a patient that we're hoping we will continue giving additional cycles. Yeah. I think maybe to add, again, we believe that CD30-positive non-Hodgkin lymphoma is a very interesting disease. We now have only two patients, so clearly too early to tell. But what is also incorporated into the amendment that Yago just mentioned that got approved is our ability to enroll up to 10 patients with non-Hodgkin lymphoma. I think at the recommended doses will clearly help us to determine also a good path forward for non-Hodgkin lymphoma. Great. This has been helpful. Thanks again. I'm showing no further questions in queue. That concludes today's question and answer session. Ladies and gentlemen, this concludes today's conference call. Thank you for participating. You may now disconnect.