Affimed N.V.
Q4 2020 Earnings Call Transcript

Published: 15 Apr 2021

[Operator:]

Good day, everyone and welcome to Affimed's Fourth Quarter and Year End 2020 Financial Results and Corporate Update Conference Call. At this time, all participants are in a listen-only mode. As a reminder, today's conference call is being recorded. I would now like to hand -- introduce your host for today, Mr. Alex Fudukidis, Head of Investor Relations at Affimed. Please go ahead.

[Alexander Fudukidis:]

Thank you, Tracy. I'd like to welcome and thank you all for joining us today for Affimed's fourth quarter and 2020 year-end financial results and operational update call.

[Adi Hoess:]

Yes. Thank you, Alex. Good day, everyone, and thank you for joining us for our fourth quarter business update call 2020. Today we'll briefly review the key developments at the company, including our recent updates on the AFM13 monotherapy interim futility analysis. And the findings presented by Dr. Katy Rezvani at AACR from the investigator sponsored clinical trial at MD Anderson Cancer Center, which is treating patients with a pre-complex combination of AFM13 and Cord Blood-derived NK cells. And we will provide an update on the clinical progress of AFM24 and our other programs currently in development. I will then hand the call over to Angus to discuss our fourth quarter financial results. We will conclude the call by highlighting some of our key milestones and week back to Affimed for the rest of this year. We are very excited to share groundbreaking clinical data with you on our programs and demonstrate progress we're making across our pipeline, which has undergone an incredible evolution in 2020 and the early part of 2021. Affimed's been a pioneer in leveraging the innate immune system to fight cancer. We have spent a good part of the last decade developing our technology, the ROCK platform, and our innate cell engagers and we're being increasing evidenced that our technology can result in meaningful benefits for patients in the clinic; a very rewarding experience for patients, their families, the doctors who treat them and for us as well.

[Angus Smith:]

I think we lost Adi but just to finish up and then move to the financials; Adi was mentioning that -- that just in case you missed it, Roivant now announced today AFM32 is being directed towards solid tumors. And in addition, we have -- want to highlight that through several recent transactions we have strengthened our balance sheet, and I will cover that in just a moment. Overall, we are encouraged with the progress that we and our partners have made and are looking forward to a promising 2021. So this is Angus Smith, Chief Financial Officer of Affimed. I will now review our fourth quarter 2020 financial results. Affimed's consolidated financial statements have been prepared in accordance with IFRS as issued by International Accounting Standard 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 the call, unless otherwise noted, will be in euros. As Adi mentioned, through several recent transactions we have been able to significantly strengthen our balance sheet, extending our cash runway, while enabling us to accelerate our multi-pronged development approach for our innate cell engager molecules. We ended 2020 with cash, cash equivalents and current financial assets of €146.9 million compared to €104.1 million for December 31, 2019. The cash balance does not include the net proceeds from our January 2021 underwritten public offering or the €10 million we received from the first tranche of the Silicon Valley Bank loan. The pro forma cash position as of December 31, 2020 including net proceeds from our January financing activities would be approximately €244.5 million. Based on our current operating plan and assumptions, including the proceeds from the recent financing, we anticipate that our cash, cash equivalents and current financial assets will support operations into the second half of 2023. Net cash used in operating activities for the year ended December 31, 2020 was €19.4 million compared to €29.1 million in 2019. Cash flow from operating activities improved in 2020 due primarily to proceeds received from the Roivant and Genentech collaborations partially offset by an increase in our net loss. Total revenue for the year ended December 31, 2020 was €28.4 million compared with €21.4 million for the year ended December 31, 2019. Revenue for 2020 and 2019 predominantly related to the Genentech collaboration. Collaboration revenue of €19.7 million for the year ended December 31, 2019 was from the Genentech collaboration. Collaboration revenue for the year ended December 31, 2020 amounted to €27.8 million or €26.2 million from the Genentech collaboration and €1.4 million from the Roivant collaboration. Research and development expenses for 2020 increased 14% from €43.8 million in 2019 to €50 million in 2020 due to higher expenses for AFM24 and other programs, as well as infrastructure investments. General and administrative expenses increased 34% from €10.3 million in 2019 to €13.7 million in the year ended December 31, 2020. The increase predominantly relates to higher personnel expenses due to the increase in headcount in 2020 and to higher legal, consulting and audit costs. Net loss for the year ended December 31, 2020 was €41.4 million or €0.50 per common share compared to a net loss of €32.4 million or €0.50 per common share for the year ended December 31, 2019. The weighted number of common shares outstanding for the year ended December 31, 2020 was 83.5 million. As of March 31, 2021, our common shares outstanding were approximately 119 million. We encourage shareholders to also review our 20-F filings for the year as filed with the SEC this morning. I will now turn the call back to Adi for closing remarks. Adi?

[Adi Hoess:]

Yes, I'm back again. Sorry for that, I was just disconnected. But thank you very much, Angus, for jumping in. In closing, I would like to reiterate our excitement document for our very important achievements in 2020. The strong start to 2021 and whole progress we are looking forward in the coming months. We've advanced our strategy of exploring our innate cell engagers as monotherapies and we're now exploring opportunities in novel combinations with NK cells in partnerships we secured with NK marks or NK chains , as they are called now. We are moving our AFM13 monotherapy study forward with both, high and low expressing CD30 positive PTCL patients. We are expecting that in the combination of AFM13 with NK cells at MD Anderson as the trial moves through the cohorts, our collaborators there will present their findings at scientific conferences throughout 2021. For AFM24, we expect to complete the dose escalation phase in our ongoing monotherapy study and initiate the dose cohort expansion phase in the second half. We are working quickly and efficiently to prepare for further investigation of combination therapies of AFM24 in solid tumors; first with engaging BIOS SNK01 autologous cell product, as well as in combination with T-cell, Roche PDL1 inhibitor. We expect to be dosing patients in both of these studies in the second half of 2021. For our pre-clinical asset AFM28, we expect to report data from pre-clinical IND enabling studies later this year, and then subsequently file the IND in the first half of 2022. Finally, there is upside. We believe there is upside in our collaborations with Genentech and Roivant because we have the opportunity to provide further meaningful updates. Updates on these programs will remain largely, however, at the discretion of our partners, and we will continue to work and support them as they move their respective innate cell engager molecules to the clinic. Now, before we open the call for Q&A I would like to say thank you to really a lot of people. So, thank you again to the patients who entrust us with their health. Very important, I want to thank all Affimed employees who are working indeed very hard and very diligently to ensure that our progress -- our programs continue to progress. And welcome and thank our new and old investors who continue to believe in us and support our scientific efforts. As always, we have the whole team on the call today, and look forward to our questions -- to your questions. Thank you very much. Operator?

[Operator:]

Thank you. Your first question today comes from the line of Joe Kim from Capital Markets.

[Joseph Kim:]

Hi, good morning. Thanks for taking my questions. Adi, you said that there wasn't any pharmacodynamic activity at the fourth dose level for AFM24. How does that align with your expectations for the dose escalation? And is there a dose level where you would stop at if you still don't see activity and just shift the development focus to combination strategies?

[Adi Hoess:]

Yes, thanks for this question. I want to hand this over to Andreas to explain where we are. But what I must say is, we have just finished the expansion of the cohort 4 and now are moving into 5; so we haven't really analyzed cohort 4. But I'll let Andreas explain you where we are.

[Andreas Harstrick:]

Yes, thank you, Adi and -- yes, the answer is in line what Adi said. We have not analyzed most of the pharmacodynamic readouts. In fact for -- for both, cohorts 3 and 4 we are using batch analyzers here. Some of the essays like CD16A we said the occupancy are quite new; so we will process the data that we have collected or the BLC samples that we have collected. So, what Adi said is, we currently do not have the data to say whether we are already at pharmacodynamically active dosing, it's a possibility that we need to evaluate over the next couple of weeks. Now, coming back to the overall strategy as Adi has shown. If we take AFM13 as a blueprint, we have seen meaningful clinical activity as a single agent in combination with PD1, as well as in combination with NK cells. According to our analysis of tumor biology, especially in the state of EGFR expressing tumors; we expect to see exactly the same picture or the same pattern. So, we believe there are distinct disease types which will benefit from a single agent approach as these patients have sufficient numbers and sufficient functionality of their own NK cells. We expect patients to benefit from our PD-1 based approach and then ultimately, there will be tumors -- solid tumors where the patient's own NK cell number in case of functionality is limited, at least initially. So, this will be patients who will be targeted with our NK cell based approaches, possibly on the long run in combination with either single agent or PD-1 plus ICE maintenance. So, it's a lot of flexibility, but we believe that we will see, as I said, the same picture with tumor entities differing in their biology and they will need accordingly different treatment approaches.

[Joseph Kim:]

Great. And I have a follow up question on the pipeline. Given that you saw strong responses with the MD Anderson study, how are you thinking about other opportunities in blood cancers and possibly revisiting CD19 but within innate cell engager or going after CD20 or CD38?

[Andreas Harstrick:]

I think these are all options that are open. Now again, CD19, CD20 is probably a field that is very well-served. We see the medical needs clearly right now in other areas, CD30 is an important area. What we just learned from the study and then when we looked closer and said CD30 expression is not only limited to T- cell lymphomas and Hodgkin's, we do see CD30 expression on B-cell especially diffused large B-cell. We also see CD30 expression in very significant chunk of acute leukemia's which gives additional options for CD30-based therapy. And as you know, we are in collaboration with Roivant and Genentech where we have not disclosed the target. So, I think the ROCK platform offers the versatility to address a number of different clinical situations. And this opportunity will expand as we go along either in-house with our new candidates or in collaboration with our partners.

[Joseph Kim:]

Understood. Congrats on all the progress and the great data that you've generated so far.

[Andreas Harstrick:]

Thank you.

[Operator:]

Thank you. Your next question comes from the line of Brad Canino from Credit Suisse.

[Bradley Canino:]

Committed to disclosing first clinical data this year, and if so, what are the factors that you're considering to determine when to present it? And then just to be clear, it sounds like you're going to continue to a Cohort 6 in the dose escalation or beyond if needed, would that be 640 milligrams? Thanks.

[Adi Hoess:]

Andreas, did you get whole question? I missed the first half.

[Andreas Harstrick:]

Yes, I missed also, probably the first. But maybe I'll start to answer from the backend and then we'll see what we what we are missing. So first of all, again, we are currently accruing at Cohort 5, possibly 20 milligrams . And as I said, we will have to analyze our pharmacokinetic and pharmacodynamic markers from the two previous cohorts. This will give us a picture where we stand in terms of pharmacodynamic activity and this will guide our decision whether to enroll additional cohorts. Now as we have also said, the relative increase of other steps, the relative increasing steps from cohort to cohort is guided by Bayesian assessment model which will suggest these relative increments from cohort to cohort based on the totality of the data we have seen over the cohorts as well as the data that we have seen in the previous cohort. So, 640 milligrams is a possibility but again, as we will collect data from Cohort 5, this may change to either a larger or a smaller increment depending on the patient analysis.

[Bradley Canino:]

Okay, great. And the first question was just are you still committed to disclosing first clinical data this year? And what factors are you looking at to consider when to present?

[Andreas Harstrick:]

Yes, a certain element of insecurity still in there. We believe that by end of this year, we should have defined our pharmacodynamic reactive dose. And as Adi said, we are also committed to start to enroll into expansion cohorts. As we said, once we have defined these pharmacodynamically active dose, we will disclose the data of the whole dose escalation part including patients' characteristics, patients' responses, as well as the pharmacokinetic and pharmacodynamic data that defines this dose selection. So our best estimate, I would say, is that all will happen within this year.

[Bradley Canino:]

Okay, thank you.

[Adi Hoess:]

I just want to reiterate, we have just finished Cohort 4. What does this mean? So, we take about four weeks for the last patient and to finish the dose escalation at that stage, we can determine the safety, and we can open to move to the next cohort. However, the assessment of such a patient is only done after eight weeks. So currently, we are analyzing data of Cohort 3 and Cohort 4, because we pulled those and that's what's been ongoing over the next week. So in essence, the way how this has moved forward is determined by really understanding the safety getting to meaningful doses, and then in parallel to the assessment. So, just to give you a little bit of an explanation of where we currently stand, and such data then could be the basis of further communications.

[Operator:]

Thank you. Your next question comes from the line of Yale Jen from Laidlaw & Co.

[Yale Jen:]

Good morning. Again, congrats on yesterday's fantastic the results. I have two questions here. The first one is, again, based on yesterday's report, do you anticipate also that for the AFM24 and SNK-01 study, that later on, you may actually preloaded the NK cell, what the engager, or you feel this is not necessarily something that's relevant for the AFM24 in solid tumor development ?

[Adi Hoess:]

We have currently disclosed as we approach this forward with monotherapy, with combination with the autologous cell product and with the anti-PD-L1 antibody from Roche. So any other activities, we're considering a number of additional options for a AFM24 at this stage amongst this, obviously, the combination with an allogeneic cell product. So, once we are have fully-validated all these steps forward, we will disclose that.

[Yale Jen:]

Okay, maybe one more question on AFM13, that last year because of the COVID, you have sort of paused the development in TMF. I just wonder with your current balance sheet and maybe a better environment, would you resume that study going forward? Or have you have any other thoughts?

[Adi Hoess:]

So currently, we have not reopened this particular arm as in most countries where we are active and COVID is still massively around. You can read this all over Europe. That's where the majority of the signs are. So, we are still in the midst of a wave and not after a wave. So, the situation hasn't indeed changed at all.

[Yale Jen:]

Okay, great. Thanks a lot. Appreciate it.

[Operator:]

Thank you. Your next question comes from the line of Daina Graybosch from SVB Leerink.

[Daina Graybosch:]

Hi, thanks for the question. I'm going to start actually asking about the AFM24 pharmacodynamics in dosing a little bit more to make sure that I understand. So, I think last time you spoke about this, the planned Cohort 5 was going to be 1,000 milligrams and now you're down at 320 milligrams. I presume what you said earlier that you have this Bayesian approach has changed what you had previously expected. And I wonder if you can get more into the details of specifically what changed from your expectations now as you actually have the data and what my explain that change? And then just to clarify on the pharmacodynamics data, so you have not done the pharmacodynamic analysis of Cohort 3 and 4, is that correct? But you did not see pharmacodynamic engagement and Cohort 2, and can you clarify specifically what the pharmacodynamic you are completing?

[Adi Hoess:]

Andreas, do you want to take the questions?

[Andreas Harstrick:]

Yes, this is a lot of questions. So, yes, I think we initially had planned and this was when we first presented the study, a relatively aggressive dose escalation step, which would have brought Cohort 5 set to 1,000 milligrams. Now already in Cohort 2, we diminished the relative increment as we wanted to make sure that we have more granularity and really can titrate the recommended dose. If you look at the relative increments, we are at are basically doubling the dose starting in Cohort 2, so that was really driven by the consideration that we need a better titration and that the initial steps might be too big. Now in terms of the pharmacodynamic, pharmacokinetic markers, what we said is that on the pharmacodynamics field, we will look at a number of cytokines and the profile of cytokines over time. We will use essays looking at the occupancy of CD16A receptors in circulating target cells, as well as some of the subsets and activation markers within the NK cells. So this is the pharmacodynamic panels that we are using. And if it was many questions, I don't know whether I missed one.

[Adi Hoess:]

I'll help you out here, Andreas. What have we seen in Cohorts 1 and 2? So, we considered those cohorts to be below the meaningful dose or a relevant dose and that's why we have been focusing on the analysis on starting with Cohorts 3 and 4. That's also the relevance that we saw, just fairly low with a dose escalation. Again AFM24 is a first-in-class innate cell engager to be developed in a solid tumor indication with a more promiscuous target. As to effects, we've seen any of the side effects that were previously reported for TKIs or monoclonal antibodies at the dose levels investigated. We've been moving straight along in this study. Again, this was all started in COVID. We've been through COVID because the vaccination around but it did impact the original cohorts in terms of how fast we could recruit. So, I guess we have made the progress for our Phase 1 program that's been at least at the level of where others have been and others indeed have reported much when difficulties of starting Phase 1 started during COVID. So, I guess that there is where we're pulling our expectations and just now at the level in order to look deeper into what we have achieved. But you're correct, now we are in Cohort 5 and the data are just coming in now.

[Daina Graybosch:]

Great. And then one other question for me. Can you talk about the rationale for an autologous NK cell therapy, which is relatively less-experienced in the academic literature for autologous? And also confirm what your starting dose will be for that combination and if you'll be dose-escalating both AFM24 and the cells or you'll be holding one constant ?

[Adi Hoess:]

I'll hand over to Andreas, again.

[Andreas Harstrick:]

I can take that. So, let's start with autologous. Yes, you're correct, there is clearly less experience and less literature about autologous. Now, when we looked at the data set, NKGen or previously NK Max has generated what we saw first if they had established a safe dose of their autologous NK cell product, and they have developed their manufacturing, their expansion capabilities in a way that allows us to use relatively high doses of NK cells on a frequent basis and can continue treatment for a pretty prolonged period of time. I believe in their current Phase 1 single agent studies, some patients have been on study in excess of half a year. Now, what we also saw, remind you, there was a small Korean study published at ASCO in patients with non-small cell lung cancer where we evaluated their autologous in case our product in combination with Pembrolizimab compared to Pembrolizimab single agent. Again, very small patient numbers. But I recall the data right, there were about four responses in treatment refractory non-small cell lung cancer patients with autologous NK cells plus Pembrolizimab. Now, we also looked at the cells in some of our in vitro assays, found them to be very suitable to work in combination with our ICE and gave us specifically was AFM24. Also taking all these data together, we believe that it is a potential expansion of our opportunities. We have an in case, a product that is safe in the clinic has an established dose has shown activity preliminary in an EGFR expressing tumor, which is non-small cell lung cancer and gives us another opportunity and basically opens a new field. So we believe it's worthwhile also to explore autologous NK cells in addition to allergenic NK cells. Now, in terms of how the study is designed, currently, the NK cell dose is fixed 4 times, 10 to the 9 NK cells, which is the dose that was established by NKMax in their single agent studies and we will have a titration of AFM24. Again, we do not necessarily have to wait for the establishment of a recommended Phase 2 dose in our single agent study. Our starting dose here for the NK cell study will be a dose levels that has cleared the safety in the single agent study. And again, we will have to assess where we are once we are ready to initiate the NK cell study which what we said will be in the second half of this year.

[Daina Graybosch:]

Thank you very much.

[Operator:]

Thank you. Your next question comes from the line of Nick Abbott from Wells Fargo.

[Nick Abbott:]

Good morning. Congratulations on all the progress and thanks for taking my questions. The first one is on the preloaded NK cells and hopefully I've got that right here. At dose level one, you've got 100% response rate at a dose that's at the low end of approved CAR-T. So, how do we think about this given that CAR-T efficacy is tied to expansion of CAR-T?

[Adi Hoess:]

Andreas, you want to take that?

[Andreas Harstrick:]

Yes, I can start and if you would chime in. So, I think what also Katy said yesterday on her call, these days are extremely encouraging. Course already was a very low cell dose, pre-complex was AFM30 and then followed by AFM30 and single agent. You see, I won't really say striking responses given also the pretreatment characteristics, the tumor load of these patients. So, this really tells us that these NK cells are with a targeted approach, can eradicate even at very small cell doses of significant tumor masses. Now, what also has been shown is that these NK cells that we are using in our collaboration with MD Anderson, are produced by the specific activation protocol, acquire some kind of memory like NK cell features, which allows them to persist for a prolonged period of time. And these are data that are just generated. So, we do have some persistence, we probably also have some proliferation. Definitely not to the degrees that CAR-T cells have. Now, the reason to go into higher doses -- and that is also what Katie alluded to yesterday -- is to deepen the responses, but also to increase the persistence of the NK cells beyond say one or two infusions that we are given and to stabilize or to prolong these responses. And then very small patient numbers, but what we have seen as with this very first patient at the higher cell dose of one times 10 to the seven, this patient went into complete response already after the first cycle. So, if you will, even more active. Again, what was specifically encouraging is that this is a patient that not only failed all of the classic pretreatment including chemotherapy, PD-1 and et cetera, but this patient in fact, has a history of having received a CD30 targeting CAR-T product and has not responded to the CAR-T product. Again, telling you that the mechanisms of action and the capability of the innate immune system and the T-cell system probably are different and I think are giving us very early, very encouraging data.

[Nick Abbott:]

Thank you. And then, I believe we have an option to license, Cord Blood NK cell technology from MD Anderson. So, how do you think about that as a strategy versus Artiva? Or does the company have the resources or interest to become a cell therapy company?

[Adi Hoess:]

Yes. I'll hand that question back to Denise.

[Denise Mueller:]

Sorry. Can you hear me?

[Adi Hoess:]

Yes.

[Nick Abbott:]

Yes.

[Denise Mueller:]

Okay, sorry. I had an issue the connection. Can you repeat the question?

[Nick Abbott:]

Yes, I believe we have an option to license the Cord Blood technology from MD Anderson. And then you also have the Artiva collaboration. So, the question is really going forward, does the company have the resources and/or interest to become a cell therapy company? Or would you continue collaborating with cell therapy experts?

[Denise Mueller:]

Yes, great question. So, as far as MD Anderson goes, we've always had the option to take the license for the worldwide rights . And at the start of the clinical study, we felt that that was the prudent time and we made the decision to take that option for the license. Such that the clinical data held and was very good that we could potentially move that forward and take that product ourselves. So, that's really providing optionality. We also really very much value our collaborations within NK Max and Artiva and those are focused in similar but different areas and provide us with a multi-pronged approach to identify optimal ways to combine our engages with NK cell therapy. And at any point in time, we could have control of obviously the MD Anderson NK cell product, or we could pursue a more strategic partnership with an NKGen -- actually, they just changed their name -- or Artiva. So we're just going to let the data drive our decision moving forward and I think it's still early days. It's very, very promising and we haven't made the strategic decision that we're 100% going to become an NK cell company. But the data is promising and will lead us to consider that at some point in the future after more data is generated from all these collaborations.

[Nick Abbott:]

Great. Thank you.

[Operator:]

Thank you. Your next question comes from the line of Yale Jen from Laidlaw & Co.

[Yale Jen:]

Thanks for picking up the follow-up questions. Just a very brief one. First one is that is there also update at ASCO for the cbNK AFM13 combo in place?

[Adi Hoess:]

Angus?

[Angus Smith:]

Go ahead, please

[Denise Mueller:]

I can take that. Yes, okay. Katie Rezvani has a session, very similar to the session that she had at AACR where it's focused on cellular therapeutics. We are not confirmed as to whether or not her panel discussion and presentation would include an update on the clinical trial that we're doing with her. But it certainly is an option. But we don't have confirmation of that just yet. It may be there, but we're not sure yet.

[Yale Jen:]

Okay. And maybe just quick one. She mentioned yesterday that if the data is still very robust going forward for the Phase 1 study, it is possible to advance to Phase 3. Any comments or your say?

[Adi Hoess:]

No, we don't want to comment on this at this stage. I guess that for the time being, we want to finish the dose escalation, identify the optimal dose for the cells and with that information, then decide on how to proceed.

[Yale Jen:]

Okay, great. Thanks. Really appreciate it.

[Operator:]

Thank you. Your next question comes from the line of Maury Raycroft from Jefferies.

[Maury Raycroft:]

Yes, good morning, everyone. Thanks for taking my questions and congrats on the progress. Just a quick one on AFM24. Just clarifying, you commented that at the initial doses, so far you're seeing a better safety profile than what you would expect with TKI or cetuximab. Just wondering if you can comment more on what differences you're referring to and would you expect that to be independent of the PD biomarkers?

[Adi Hoess:]

Andreas?

[Andreas Harstrick:]

Yes, as we said, we would like to present all the data raw once we have established pharmacodynamic active dose. What we can see is that we have not seen some of the hallmark side effects, for example, skin toxicity or magnesium losses or so, which you would expect with the EGFR. But again, as we progress through, we will collect more data. But I think it's so far in-line with our preclinical study, especially the cynomolgus monkeys, reminds they are even with the highest dose, we did not see any, for example, skin toxicities, which is in-line with the completely different and innovative mechanism of action of this drug. And the second question, the second part was, again, relating to PD? Can you repeat it?

[Maury Raycroft:]

Yes, just wondering if the safety effects I guess you viewed, is that independent of the PD biomarker assays that you're doing? Or should they kind of go hand-in-hand?

[Andreas Harstrick:]

Yes, I think we -- again, based on the mechanism of action and on the PD panel, we would not expect to see a direct correlation between any potential side effects and NPD markers. It's a new field, but again, the NK cell, as we have learned from AFM13, also from Katie's study. It's pretty focused, I would say, and -- while we have not seen and in all of our NK projects, for example, or significant organ toxicities, and we expect that the same will be true for AFM24.

[Maury Raycroft:]

Got it. Okay, that's really helpful. And then, one quick question on AFM13 pivotal study in PTCL. Just wondering, if at this point, if you guys could provide any more clarity on enrollment expectations and whether the final data could be second half of this year or first half of '22?

[Adi Hoess:]

Andreas, you want to take that?

[Andreas Harstrick:]

Yes, yes. Firstly, what Adi mentioned already around cohorts is, the TMF cohort -- we are still in the middle of the pandemic situation, U.S. is getting a little bit better but Europe is still heavily infected. So, as we said already during the interim analysis or around the interim analysis, currently we do not feel comfortable to give a very concrete date in terms of enrollment. Remember, protocol mandated cohort B was on hold while we were conducting the interim analysis; so cohort B has now been reopened. But I think it's too early to assess the full impact, and then make a concrete prediction of the timeline. So, I think if we -- if we have reopened cohort B for a little bit longer time and we have a better grasp on the COVID situation, we should be in a position to give you a more granular answer than we can right now.

[Maury Raycroft:]

Makes sense. Okay, thank you for taking my question.

[Adi Hoess:]

Thank you very much. And I guess there are no further questions, correct?

[Operator:]

We have no further questions. So, if you wish to continue.

[Adi Hoess:]

Yes. Thanks very much. I just want to thank all, everybody who was attending today for their listening in and questions. And look forward to further updates in the next six to nine months as we proceed. And wish you all have a nice day and subsequent good meetings with us. Thank you. Bye, bye.

[Operator:]

Thank you. That does conclude your call for today. Thank you all for participating. And you may now disconnect.