Good day, and thank you for standing by. Welcome to the Affimed First Quarter 2021 Financial Results and Corporate Update Conference Call. At this time, all participants’ lines are in listen-only mode. [Operator Instructions] After the presentation, there will be a question-and-answer session.

[Operator Instructions] Please be advised that today's conference may be recorded. I’d now like to turn the conference over to your host today, Mr. Alexander 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 for our first quarter 2021 results and operational update call. Before we begin, I'd like to remind everyone that we issued the relevant press release earlier today and that it can be found on the Investor Relations section of our website.

On the call today, we have our management team, Dr. Adi Hoess, our Chief Executive Officer; Andreas Harstrick, our Chief Medical Officer; Arndt Schottelius, our Chief Scientific Officer; Wolfgang Fischer, our Chief Operating Officer; and Ms. Denise Mueller, our Chief Business Officer; and Angus Smith, our Chief Financial Officer.

The whole team will be available for the Q&A session. Before we start, I will quickly go through the Safe Harbor statement. Today's discussion contains projections and forward-looking statements regarding future events. These statements represent our beliefs and assumptions only as of the date of this call.

Except as required by law, we assume no obligation to update these forward-looking statements publicly or to update the reasons why actual results could differ materially from those anticipated in the forward-looking statements, even if new information becomes available in the future.

These forward-looking statements are subject to risks and uncertainties and actual results may differ materially from those expressed or implied in 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?.

Thank you, Alex. Good day, everyone, and thanks a lot for joining us today for our first quarter update call. I will provide updates on our pipeline and discuss the progress of our ongoing studies, in particular, for AFM13 and AFM24, and our plans for the remainder of this year.

I will also speak briefly about the announcement of our partnered BCMA program with Genentech. I'm very pleased to report that we are maintaining our momentum by continuing to execute well across all of our wholly-owned programs.

We’re leveraging the unique features of our innate cell engagers, which we also call ICE across different programs and have continued to publish data that support the multi-pronged approach of our development strategy, which includes development of our ICE as monotherapy, and in combinations with natural killer cells and in combination with PD-1 or PD-L1 checkpoint inhibitors.

Our AFM13 and AFM24 clinical programs are on track. Let me start with the registration-directed study of AFM13. This study is conducted as monotherapy in relapsed/refractory peripheral T-cell lymphoma, and we continued to enroll patients following the positive interim analysis outcome, which we reported in March of this year.

Today, we announced that we expect to complete enrollment of about 110 patients in the first half of 2022, and that we expect to be able to provide guidance about timing for data as we get closer to the completion of enrollment. We are also very pleased with the progress in the enrollment of the Phase I study at MD Anderson Cancer Center.

This study is evaluating increasing doses of cord blood-derived natural killer cells pre-complexed with AFM13. Today, we reported that the dose escalation cohorts are now fully enrolled and that we expect MD Anderson will have a data update from this study at a major medical conference in the second half of this year.

In the current protocol of the study, patients can receive up to two cycles of therapy. A cycle consists of one infusion of AFM13 pre-complexed with cord blood-derived natural killer cells followed by three weekly administration of 200 milligram of AFM13 monotherapy.

The dose of natural killer cells is 10 million per kilogram of body weight in cohort 2 and 100 million per kilogram of body weight in cohort 3. In April, Dr.

Rezvani of MD Anderson Cancer Center presented data on the first four patients that were treated with this therapy and each experienced significant disease reduction, with two complete responses and two partial responses, an objective response rate of 100%.

In May, we announced the publication in Clinical Cancer Research supporting the therapeutic potential of AFM13 in combination with natural killer cells. Arndt, our Chief Scientific Officer, will discuss the key takeaways from the publication in some of our other preclinical work in just a few minutes.

Important to us, AFM13 continues to validate our three-pronged development strategy for our innate cell engager molecules. We've now demonstrated that we can drive responses as monotherapy in indications where the innate immune system is functional. Here specifically, we mean peripheral T-cell lymphoma.

We further published data on the combination of AFM13 with pembrolizumab that demonstrated synergy between AFM13 and PD-1 inhibitor in Hodgkin lymphoma. And we have emerging data and emerging dataset around the combination of AFM13 with cord blood-derived NK cells that had demonstrated exciting initial results in CD30-positive lymphoma.

The data was now generated from AFM13 is informing the way we develop the rest of our pipeline, notably AFM24 and AFM28. Let me turn to AFM24. Development of AFM24 is on track. In our ongoing monotherapy study of ill patients with advanced EGFR-positive solid malignancies.

The aim of this dose escalation phase of the study is to determine the maximum tolerated dose and the establishment of a recommended Phase II dose. The dose expansion phase is intended to collect preliminary evidence of efficacy in specific indications and to further confirm the safety of AFM24.

As announced today, we’ve now completed dose cohort 5 at 320 milligram and recruitment of patients into cohort 6 has begun at a dose level of 480 milligrams, which is a 50% increase in dose from cohort 1. The decision to increase to 480 milligrams was driven by data derived from the cohort 1 to 5.

Specifically, our decision was informed by pharmacodynamic data from cohorts 1 to 4 and pharmacokinetic data from cohorts 1 to 5.

Key and indeed very encouraging findings are that we are seeing a more than dose-proportional increase in exposure as we escalate the dose, and the increase in exposure is now correlated with increases in activation markers on natural killer cells and CD16A receptor occupancy. Importantly, we have not observed times of NK cell exhaustion.

In terms of safety, no medical relevant drug-related side effects has been reported other than infusion-related reactions, which are managed to stand the pre-medication. We have indeed not seen any of the classical EGFR-related toxicity to cohort 5, such as skin or other organ toxicity.

Subject to additional dosing steps, we plan to determine the recommended Phase II dose, and we are expecting to begin the expansion cohorts in the second half of this year.

Now in parallel, we are making progress towards our goal of beginning two additional combination clinical studies, which would include the investigation of AFM24 in combination with Roche anti-PD-L1 antibody atezolizumab by leveraging now both the innate and the adaptive immune system, we believe we can potentially show synergistic effect [indiscernible] for AFM13, and this could provide a very meaningful benefit to patients.

We expect to dose the first patient in a Phase I/IIa study evaluating the combination in the second half of 2021. In addition, we expect to initiate a Phase I/IIa study for the combination of AFM24 with NK Gen bios autologous NK cell product in the second half of this year.

We are committed to pursuing our multi-pronged development strategy, developing the approach for AFM24, which we believe will enable us to target a broad range of EGFR-expressing tumor types and population indeed all at the same time.

For each of our three AFM24 studies, we plan to have expansion cohorts in at least two to three different indications. In total, the AFM24 program will target a broad range of EGFR-expressing tumors, providing us with multiple opportunities for clinical success.

We expect to disclose more details about the indications for these studies later this year. Let me talk about – quickly about AFM28, our third program. For AFM28, we continued to advance the IND enabling studies and we plan to release information about the target and initial preclinical data at the major medical conference later this year.

We need to remain on track to submit the IND application in the first half of 2022, and our goal is to begin our clinical study in the second half of 2022. This morning, we also announced an update on the development of RO7297089 by our partner Genentech. This is the BCMA-targeting innate cell engager.

Genentech has completed the dose escalation portion of the Phase I study. No dose limiting toxicities were observed during the study. However, due to a broader portfolio consideration, Genentech decided to stop the Phase I study.

As a reminder, this program was only the first of multiple targets under development with Genentech, and they made it clear to us that this decision does not have any implications for our platform or impact the continued development of the other targets.

So we should remain – we are remaining confident in our collaboration with Genentech and look forward to progressing the additional targets towards clinical development. Now I'd like to leave you with a message today that we are very proud and excited to be able to play a leading role in developing cancer therapies based on innate immunity.

As we have shown at multiple events, we believe that our innate cell engager molecules offer unique advantages over other immunotherapies. They do this by binding to a unique epitope on CD16A, which allows us to show a reduced competition with plasma HEG leading to a far more effective tumor cell killing with ADCC and ADCP.

They have superior binding and retention on natural killer cells which have been shown to persist over several days. They are able to kill tumor cells independent of the level of antigen expression, and now being shown that in case of preloaded or pre-complex with our high affinity innate cell engagers showed improved tumor cell killing.

We have positioned Affimed in a unique place in the innate immune cell therapy landscape. We have developed the differentiated ROCK platform that generates innate cell engager molecules, enabling NK cells and macrophages to locate the tumor, and once they do to eliminate it.

Furthermore, as we are learning [indiscernible] NK cell-based approaches, these require the specific targeting of NK cells to recognize the tumor cell. We are addressing this important need with our bispecific innate cell engager molecules. With that, I’ll hand over the call to Arndt. After Arndt, Angus will give you an update on our financials.

Arndt?.

Thank you, Adi, and good morning, everyone. Also, warm welcome for me. As Adi mentioned, in the past few months, we have generated exciting preclinical data with our ICE molecules, which I'd like to share with you today. On AFM24, we presented a preclinical poster at this year's AACR.

In that poster, we were able to demonstrate that AFM24 in combination with adoptive NK cells leads to a AFM24 dose-dependent tumor regression in a mouse xenograft model establishing a strong pre-clinical proof-of-concept for this promising combination.

This important finding was further supported by data demonstrating that AFM24's ability to tightly bind to NK cells as well as its cytotoxic potential to kill EGFR-expressing tumor cells was unaffected by the presence of competing IgG. This is in contrast to cytotoxic potential which was greatly diminished by completing IgG.

The poster further showed that AFM24 induces a very prominent ADCP response or killing through macrophages against EGFR positive tumor cells irrespective of the presence of KRAS mutations further adding why we believe this is a highly differentiated drug candidate.

On AFM13 in a collaboration with Björn Önfelt at the Karolinska in Stockholm, we generated data demonstrating that the addition of AFM13 to NK cells renders these NK cells serial killers.

If you look at Slide 6 in your presentation that shows microscopy pictures of a single well containing a single NK cells and multiple tumor cells in the absence and presence of AFM13. On the top row, you can see that the single naked and undirected NK cell, which is shown in blue, is not able to kill CD30-positive tumor cells.

Those are shown in red over time period of 12 hours. The video capturing activity at each time point shows that the naked NK cells without the addition of AFM13 moves around in an undirected fashion without killing tumor cells and stark contrast.

And as shown on the lower line of pictures, the addition of AFM13 clearly increased the ability of that NK cells not only to kill one, but several tumor cells.

They are turning from red to green when they are being killed, demonstrating that the innate cell engager AFM13 effectively directs NK cells to tumor cells and can render these NK cells serial killers.

Next, I would like to summarize the key findings of our collaboration with the labs of Katy Rezvani at MD Anderson; Todd Fehniger, 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, including cytokine-activated or cord-blood derived NK cells, resulting in enhanced tumor recognition and ADCC, antibody-dependent cellular cytotoxicity.

This exciting data formed the basis for the successful IND of the ongoing Phase I study with pre-complexed cord-blood derived NK cells at MD Anderson in patients with CD30-positive lymphomas.

The schematic on Slide 7 shows that cord-blood derived NK cells were pre-activated in the presence of IL-12, IL-15 and IL-18 for 16 hours are were left untreated before being further co-cultured with the feeder cells, resulting in expanded cord-blood NK cells shown on the top of the schematic are resulting in preactivated and expanded or abbreviated later as P and E, P+E cord-blood derived NK cells which are shown on the bottom.

As you can see on the next Slide 8, on the right, the cytotoxic efficacy of preactivated 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, which are shown in light blue.

Importantly, the surface expression of CD16 remains unaltered in both treatment groups as you can see on the graph on the left.

If you go to Slide 9, shows you on the right that the long retention on NK cells after preloading these with AFM13 leads to a substantially higher degree of specific killing of CD30-positive tumor cells over a 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. And this is the comparison between the blue and the red bars. The graph on the left shows that this AFM13 mediated high degree of cytotoxicity monitored frequently over a period of 24 hours.

Also, in this graph, we can clearly see that the degree of ADCC is much higher in AFM13 preloaded versus unloaded preactivated and expanded cord-blood derived NK cells.

And again, that washing the NK cells complexed with AFM13 does not affect their ability to kill, 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.

Indeed, we can generate these CAR-like NK cells in just one to two hours. I will now turn the call over to Angus to provide an update on our financial position and quarterly results.

Angus?.

Thank you, Arndt. Affimed consolidated financial statements have been prepared in accordance with IFRS as issued by the International Accounting Standards Board or IASB. The consolidated financial statements are presented in euros, which is the company's functional and presentation currency.

Therefore, all financial numbers that I will present in this call, unless otherwise noted will be in euros. We ended the first quarter of 2021 with cash and cash equivalents of €240.7 million compared to €146.9 million on December 31, 2020.

The cash balance includes the net proceeds from our January 2021 underwritten public offering and the €10 million we received from the first tranche of the Silicon Valley Bank loan.

Based on our current operating plan and assumptions, including the proceeds from the recent financing, we anticipate that our cash and cash equivalents will support operations into the second half of 2023. Net cash used in operating activities for the quarter ended March 31, 2021 was €16 million compared to €16.5 million in the first quarter of 2020.

Total revenue for the first quarter ended March 31, 2021 was €11.7 million compared with €5.1 million for the quarter ended March 31, 2020. Revenue for the first quarter of 2021 mainly comprised of collaboration revenue from Genentech and Roivant.

Research and development expenses for the first quarter of 2021 remained flat at €11.4 million compared to the first quarter of 2020. General and administrative expenses for the first quarter of 2021 increased to 27.3% to €4.5 million from €3.5 million in the first quarter ended March 31, 2020.

The increase relates largely to higher personnel expenses, higher premiums for our D&O liability insurance and higher legal and consulting expenses. Net finance income for the quarter ended March 31, 2021 increased by 242% from €1.6 million in the quarter ended March 31, 2020 to €5.5 million.

This increase is largely due to foreign exchange gains related to assets denominated in U.S. dollars as a result of the strengthening of the U.S. dollar against the euro during the first quarter.

Net income for the quarter ended March 31, 2021 was €1.4 million or €0.01 per common share compared with a net loss of €8.3 million or a loss of €0.11 per common share for the quarter ended March 31, 2020. The weighted number of common shares outstanding for the quarter ended March 31, 2021 was 116.2 million.

I will now turn the call back to Adi for closing remarks.

Adi?.

For AFM13, we expect to complete enrollment in this study in the first half of 2022 and to provide guidance for the timing of the data release closer to the time when we complete the enrollment in this study.

For the study of AFM13 pre-complexed with NK cells, we expect that the team at MD Anderson Cancer Center will record additional data at our major medical conference in the second half of this year.

For AFM24 monotherapy, we are now recruiting in dose cohort 6 and are on track to complete the dose escalation and start our expansion cohorts in the second half of this year.

We further expect to initiate two Phase I/IIa combination study for AFM24 in the second half of this year, including the study with NKGen, SNK01 NK cell therapy and that study in combination with Roche Tecentriq.

For AFM28, we expect to disclose the target for this program and publish initial preclinical data at a medical conference in the second half of this year.

I'd like to reiterate our appreciation and gratitude to our investigators and [indiscernible] patients and their families and our employees across the organization for their continued support and commitment in our efforts. We would now be happy to take any questions that you might have.

Operator?.

[Operator Instructions] Our first question comes from Maury Raycroft with Jefferies..

Hi. Good morning, everyone, and thanks for taking my question. So first question is just if you can talk more about where you are at with PD in cohort 4 for AFM24.

I guess if you use a positive control or think about maximum NK cell activation markers in CD16A occupancy, where are you at for with the PD for dose level 4 and how much more room do you have to go?.

Andreas, can you take this question, please?.

Yes. Sure. So what we have said is that we see significant increases in exposure, which is more than dose proportional and that the activation markers that we are looking at that include CD16 receptor occupancy, but clearly not limited to CD16 receptor occupancy or – show a good correlation with the exposure.

So as we go up, we expect to get into the range of pharmacodynamically optimal dose. That was one of the reasons why we decided to go to – in a smaller step now. So instead of a 100% increase, we selected to go with a 50% increase. Again, we are very happy with the safety profile.

As we have announced, we have not seen any of the typical organ toxicity, most notably skin toxicity or any other medically relevant toxicity. So we are titrating the dose to really define the optimum biological dose. And this was the reason why we decided to go into smaller steps..

Got it. That's helpful and makes sense.

And based on your objectives for AFM24 to pick a recommended Phase II dose based on the demonstrated ability to improve outcomes, I guess, can you clarify if you plan to continue exploring higher doses until you see a safety issue or see exhaustion of NK cells or are there specific efficacy parameters that you're looking at with the monotherapy?.

Yes. Good question. So as we have said previously based on the mechanism of action and the preferential activation of NK cells in tumor tissue. We would not expect and also in line with our cynomolgus monkey data, we would not expect to encounter any classical dose limiting toxicity.

So we will probably not escalate to see toxicity because this is probably a very unrealistic high dose. What we will monitor closely are the pharmacodynamic markers.

As we said, we have a mixture of markers that indicate activation of cNK cells looking at CD16 receptor occupancy, but also monitoring NK cell exhaustion and we will titrate the dose that we get a maximum increase in the activation marker, while maintaining a functional NK cell, so minimizing the exhaustion markers, and this will guide us in our selection for our dose that goes forward into the Phase II and then to the expansion cohorts..

Got it. That's very helpful. And then last question, based on the PD data from cohort 4 and the PK data from cohort 5.

Can you say if it's possible that cohort 5 dose level could be sufficient to start the combo studies in the second half of 2021?.

I think it's a little bit too early. As we said, we believe that we should be able to define the recommended Phase II dose second half of this year versus cohort 5 or maybe one dose cohort above, we'll still depend on the data that we are seeing..

Got it. Okay. Thank you for taking my questions..

You're welcome..

Our next question comes from Daina Graybosch with SVB Leerink..

Hi, thank you for the question. I'd like to talk more about the Genentech decision. And I guess one logistical question or process question, and one science question. So I'll start with the process question.

Do you – can you – do you plan to take this program back as AFM26 and will we – will Genentech present the dose escalation results for the medical conference?.

Yes. Thank you, Daina. I will hand over to Denise, she is mostly in contact with Genentech team..

Yes. Hi, Daina. Thanks for the question. This is really early news for us, and we haven't discussed with Genentech what the future of the program could look like, including whether or not rights could revert back to Affimed. It's just too early on that.

But what we do know is Genentech will be planning on publishing the data at a medical conference later this year..

That's helpful. And scientifically, it struck us to remember that we've seen or we haven't seen promising results of NK cell therapy, adoptive cell therapy in multiple myeloma.

I believe the Gamida cell had a cohort of their NK cell therapy combined with elotuzumab that they never presented, but suggested that the results weren't particularly promising.

I wonder if you could scientifically put this in context for what we've seen for other NK cell, either NK cell therapy or NK cell-directed therapies in multiple myeloma?.

Yes. I’ll turn this over to Arndt and Andreas. Andreas, I think, you could start.. You could address, please..

Yes. I think it's a good question. I think what is important to note is that we do not know anything about the efficacy in the Phase I study. So we have not seen the full dataset other than our exchange of safety information. So this is probably a little bit too early to speculate about efficacy or loss of efficacy.

In general, I would agree multiple myeloma appears to be a difficult area for immune-based therapies. It's not only in NK cell approaches so far where we're not so successful. We also can recall the failure of PD-L1 in multiple myeloma.

So it appears to be a very specific biology really – probably differing a little bit from biology and other lymphoid malignancies. But again, as we do not have the full dataset, it would be premature to speculate really, yes..

Got it. So we should not assume – go ahead. Sorry..

No, no, Daina, please you go ahead..

I'd like to hear what you were going to add.

And I just wanted to summarize that we really shouldn't assume the efficacy results?.

Yes. I mean, just the one thing I would add, the Gamida, it's interesting, I would say, it's probably except elotuzumab is not one of those stronger antibodies kind of in the field with NK cells, so that could have a bearing there and really nothing to add what Andreas has beautifully explained about also immune function in multiple myeloma..

Okay, great. And then one last question here.

Do you have any sense of when we could learn the target or when you will announce the targets for other programs in the Genentech collaboration?.

Hi, Daina, it’s Denise. We're prohibited from disclosing anything related to the targets with Genentech, and I guess it would become apparent when they take one of the next molecules into the clinic, at which point in time it will be apparent. But unfortunately, we're not able to disclose any of those.

What I can tell you is it's a mix of solid and hematologic targets that we're working on with them..

Great. Thank you very much for answering the question..

Our next question comes from Nick Abbott with Wells Fargo..

Good morning. Thanks for taking my question. On AFM24, I seem to recall in preclinical models at least in and this is – I guess a general observation with innate cell engagers that you see cleavage of CD16 after binding.

And so as you look at the data that you're accumulating the PD data, and I don't know, I can't remember if that leads to soluble AFM24 CD16 or soluble CD16 AFM24 complex.

But – are you seeing this, are you able to look at this and look at that expected cleavage event? And then allied to that, do you seeing evidence of any NK cell margination and how do you think about total NK cells versus circulating NK cells or the circulating pool as you think about optimizing that pharmacodynamic endpoint?.

Arndt, can you take that question?.

Sure. Yes. Nick, great question. Thank you. First of all, we can to some degree. Look at cleavage not so clearly in the patient, but what we have seen as you noticed in preclinical models that is not affecting. First of all, it doesn't really – we don't see that to a certain degree.

It's not affecting the efficacy of the molecules acquired in contrast and we have commented previously, we believe that some degree of cleavage that we have observed is probably good biologically because it enables also the NK cell to disengage and engage again.

Again, when we look at what we have seen in our – really describing with Björn Önfelt, and this is just a preview of something we want to publish more substantially towards the end of the year, we see the ICEs render the NK cells serial killers.

And that again, I think has also to do to some extent with the ability to disengage and some amount of cleavage. Now to your question about margination of NK cells overall numbers and what we have seen, let's start with the preclinical studies. If you may, you recall the monkey data, we have seen that the peripheral levels transiently go down.

We believe that is most likely margination with the cells coming back. It also, we believe is a sign of the NK cells actually being led into the tumor. So also more generally we think there's two mechanisms of action. Of course, that would be expected.

One, the innate cell engager leading the NK cells from the periphery into the tumor, and the innate cell engager also taking the NK cells in the [tumor microenvironment] and really engaging them to kill the tumor. Let me stop here just to make sure that I'm answering your questions..

Yes. I think we're definitely getting a lot of good information.

But as you sort of think about that threshold that you want to see in PD, are you able to account for these different pools, the tissue RET, the NK cells in tissue versus circulating NK cells and that movement presumably between those two pools?.

Yes. We are – I think we have said that we're looking at [site off] as we look at the activation markers, exhaustion markers, of course, look at all of the NK cell populations very actively in this study, we will also be able to some extent looking at [indiscernible] and see what kind of infiltration we get into the tumor.

So there will be an evolving overall picture in terms of distribution of NK cells..

Okay. Great. Thank you very much..

Thank you, Nick..

Our next question comes from Yale Jen with Laidlaw & Company..

Good morning, and thanks for taking the questions. My first question is that a little bit forward-looking one. In terms of AFM13 monotherapy, once you complete a current study, my understanding is that you later conducted a confirmatory study.

My question is that, would you potentially start a confirmatory study before you have the readout of the current study or you would do that afterwards?.

Andreas, that's a question for you..

Yes. We have not finalized this. As you know, we are targeting an accelerated approval with 202, which would require us to start or to have a confirmatory study at the time of CLA submission.

So this was something I think where we started to engage with FDA into discussions, not only about the monotherapy program, but again about the broader AFM13 development strategies that could include NK cell-based therapies as well as monotherapy.

So it's something that we need to do as we are approaching the completion of the enrollment phase, but we have not made a final decision here..

Okay. Great. And maybe two quick questions.

The first one is that although I understand the AFM13 combo – NK cell combo that is still ongoing, but given that today the open label one, so is there any read through at this point for your design for the AFM24 NK cell combo study at the moment?.

At the moment we are pursuing two different strategies. As you know, AFM13 uses allogeneic product, and we are employing our preloaded NK cells. Now for AFM24, we use autologous NK cells. So the SNK-01 product from NKGen, which has already established safety profile has also shown some preliminary activity.

Here we are really looking at co-administration, so parallel infusion. We are giving the NK cells much more frequently. We're giving NK cells on a weekly basis. We also have a significantly higher total number of NK cells.

So if you will, we are more or less exploring the broad spectrum that you could think about from one NK cell infusion allogeneic preloaded to multiple NK cell infusion autologous and co-administration and really see how these disease strategies will differ, which would guide us in all the way forward.

But currently they are quite different, testing really two different strategies..

Okay. Maybe the last question, you mentioned about checking the NK cell exhaustion, probably marker, probably it’s an important one across the board at this point. Would you provide a bit more color in terms of what specific sets of biomarkers are the key to pay attention – for investor to pay attention to? Thanks..

Arndt, do you want to take that question?.

Yes. Happy. So Yale, I know as NK cell expert, you will be interested in like everybody else. We are not disclosing that at this time. Also, please understand that could have also IP implications. And of course, we want to share that entirely.

We can tell you that, of course, we all – that's a pretty broad panel and includes all of the markers that you would traditionally expect in terms of activation and all exhaustion. So that's as much as we can say at this time..

Okay. I really appreciate that, and I really fully understand that. And again, congrats for heading into the second half of this year..

Thank you, Yale. Thank you..

[Operator Instructions] I'm showing no further questions in queue at this time. So that will conclude today's question-and-answer session. Ladies and gentlemen, this concludes today's conference call. Thank you for participating. You may now disconnect..