Thank you, Serena. Thank you for joining us today for Affimed's Conference Call to discuss the Company's First Quarter 2019 Financial Results and Operational Progress. This morning Affimed issued a press release, which is posted on the company's website at www.affimed.com.

On the call with me today are Adi Hoess, Chief Executive Officer of Affimed; Florian Fischer, Chief Financial Officer. Also with us on today's call and available for questions are Leila Alland, Chief Medical Officer; and Wolfgang Fischer, Chief Operating Officer, who oversees our regulatory efforts.

We will begin today's call with opening remarks from Adi on our strategic focus and progress during the first quarter, and then, Florian, will review the financial results. Following the prepared remarks, we will host the Q&A session. Before we start, let me review our 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 discussion.

Except as required by law, we assume no obligation to update these forward-looking statements publicly or to update the reasons why the 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 the forward-looking 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 Cautionary Statements Regarding Forward-looking Statements in our Form 6-K filed with the SEC earlier today.

With that, I will now turn the call over to Adi..

Thanks, Greg. Good morning, everyone, and thank you for being with us. Affimed intends to broaden its leadership position in innate immunity-based cancer therapies. We, therefore, conducted a strategic review of our development programs.

We assess the target disease indications and unmet medical needs, commercial opportunities as well as the clinic and regulatory paths to approval.

Following completion of this internal review, we believe even more strongly that our innate cell engagers has the potential to transform current immuno-oncology approaches by actualizing the untapped potential of the innate immune system, to give patients back their innate ability to fight cancer, thereby addressing unmet patient needs in treating hematologic and solid tumor malignancies.

As a result, we have determined that the optimal use of our resources at this time is to focus our research and development investments on advancing ongoing and previously announced clinical trials for our CD16A-targeting innate cell engager candidates, including AFM13 and AFM24.

In line with the strategic focus on our innate immunity portfolio, we have made the decision to terminate the Phase I clinical programs of AFM11, a CD19/CD3-targeting bispecific T cell engager.

This decision took into consideration the competitive landscape of T cell directed therapies currently in development and associated resources needed for further development of AFM11. In May, we received notification from the FDA that additional data would be needed to determine whether the AFM11 clinical hold may be lifted.

We have informed the FDA of our intention to terminate the clinical program. Indeed, our R&D strategy is based on time and cost-efficient drug development with the aim of providing safe and effective innate cell engager-based therapies to patients.

In particular, we are focusing development of our innate cell engagers on indications with high unmet need and the potential for a rapid path to regulatory approval.

An example of this strategy is our planned registration-directed study of AFM13 monotherapy in relapsed and refractory peripheral T cell lymphoma and transformed mycosis fungoides, which we believe represents a potential streamlined path to commercialization for AFM13 and a substantial commercial opportunity for Affimed.

We're currently aiming at the second half of 2019 to start this study, following agreement with the FDA on the final study protocol. We are also focused on exploring rationale combinations of our innate cell engagers with other therapeutic modalities such as adoptive NK cell therapies and Ipos [ph] products including checkpoint inhibitors.

An example of these efforts is our work with the MD Anderson Cancer Center and their investigator-sponsored study directed towards development of an off-the-shelf adoptive immunotherapy comprised of AFM13 premixed with MD Anderson's expanded cord blood-derived allogeneic NK cells in patients with relapsed/refractory CD30-positive malignancies.

As you may recall, MD Anderson presented data supporting the rationale for such a study at the ASH Annual Meeting 2018.

Such data described the successful development of a novel premixed product of expanded allogeneic cord blood-derived NK cells preloaded with AFM13 to redirect the specificity of NK cells against CD30-positive malignancies in preclinical models as well as in vivo data confirming the antitumor activity of these AFM13 NK cells.

Of note, we have recently seen other novel NK cell-based cellular products entering early-stage clinical studies and we believe such products could offer additional combination opportunities for our innate cell engagers.

During the first quarter, we presented new data on preclinical advances with AFM13 at the American Association for Cancer Research Annual Meeting that further substantiates the rationale for combining AFM13 with adoptive NK cell-based therapies.

With our collaboration partners from Washington University School of Medicine, we presented data describing functional responses of conventional and cytokine-induced memory-like NK cells in the presence or absence of AFM13.

In particular, applying functional mass cytometry AFM13-triggered functional responses were evaluated at single-cell resolution providing important insights into the AFM13's effect on NK cells on a molecular level.

The combination of these cytokine-induced memory like NK cells with AFM13 potentiated cytokine secretion and cytotoxicity towards tumor target cells. Looking ahead, we anticipate further progress with clinical data updates on AFM13 from the completed combination study with Keytruda and ongoing monotherapy investigator-sponsored study.

Abstracts providing updates on these AFM13 clinical studies have been accepted for oral and poster presentation respectively at the upcoming 15th International Conference on Malignant Lymphoma in June in Lugano, Switzerland.

Now let's turn to AFM24, our second innate cell engager product candidate and a potential treatment for multiple solid tumor malignancies. We continue to anticipate completing IND-enabling studies of AFM24 by mid-2019 to support the initiation of the first-in-human study of AFM24 in the second half of 2019.

AFM24 is designed to treat patients with EGFR expressing solid tumors by using a novel differentiated mechanism of action that activates innate immunity i.e. natural killer cells and macrophages, rather than working through inhibition of EGFR mediated signal transduction.

We see strong potential for development of AFM24 in multiple indications given that EGFR is expressed in several tumor types including CRC non-small cell lung cancer, head and neck squamous cell carcinoma glioblastoma and others.

Underscoring the need for novel therapies directed against EGFR such as AFM24 are recently reported unsuccessful attempts with modalities based on entirely different modes of action. So there is a large number of patients that currently have very limited options. We presented new preclinical data of AFM24 at the AACR Annual Meeting.

The data highlighted the differentiating features of AFM24 versus standard-of-care anti-EGFR therapies such as cetuximab including tumor cell killing independent of RAS mutational status induced tumor lysis through antibody dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis as well as toxicology studies demonstrating a favorable safety profile.

In detail, AFM24 did not elicit any side effects such as skin or gut toxicities at doses which were about four to five times higher than what have been reported for standard-of-care anti-EGFR therapies, which are associated with heavy cytokines.

Pre-clinically, we have shown increased in vitro potency directed against cells with high and low EGFR expression levels. Furthermore, we believe AFM24 has the potential to treat a broader group of patients as compared to standard-of-care anti-EGFR therapies, which are active only in subsets of EGFR-expressing tumors.

For example, we have shown pre-clinically that AFM24 is able to eliminate tumor cells that are also destroyed by monoclonal antibodies such as cetuximab.

But importantly, AFM24’s key potential differentiation is that it could also provide a therapeutic option for patients who are eligible for novel therapies aimed at treating the KRAS mutant population.

KRAS is an important regulator in the EGFR signaling cascade and it has been reported that patients with mutated KRAS do not respond well to treatment with signal transduction inhibiting monoclonal antibodies like cetuximab and panitumumab. Pre-clinically, AFM24 has shown activity toward EGFR-expressing cells harboring KRAS mutant.

In addition to AFM13 and AFM24, we're also working toward expanding our early clinical stage pipeline that generate in proprietary novel innate cell engagers based on our fit-for-purpose ROCK platform that address hematologic and solid tumor malignancies.

Additional efforts in this area include both under our ongoing collaboration with Genentech, where we are developing novel NK cell engager-based immune therapeutics to treat multiple cancers.

During the first quarter, we received a payment from Genentech in an undisclosed amount triggered by the achievement of a preclinical milestone under our collaboration thereby strengthening our cash position from a non-dilutive source.

Next, I want to briefly comment on the advantages of our CD16A directed innate cell engager ROCK platform and products, which we believe differentiates us from other approaches.

Historically, better survival was reported for certain monoclonal antibodies in patients expressing a specific variant of the CD16A receptor on innate immune cells the so-called high affinity CD16A receptor. This version is characterized by the valine-valine combination of amino acids at position 158.

Patients expressing valine/phenylalanine or phenylalanine variance have lower affinities to these monoclonal antibodies resulting in shorter overall survival. Strategies aiming at addressing the 158 polymorphism with a high-affinity approach have recently been reported to show a significant PFS and survival advantage in such patients.

We have pre-clinically demonstrated that the CD16A ROCK platform can effectively target all polymorphic CD16A 158 versions equally and this with an even higher affinity and selectivity as compared to other approaches. So overall, this could result in increased efficacy in any population independent of the 158 polymorphism.

Lastly, I want to comment on the management change that we announced in this morning's press release. Dr. Martin Treder will step down from his position as Chief Scientific Officer to pursue other opportunities. He will continue to support Affimed as a consultant.

Martin made significant contributions to the development of our ROCK platform the foundation of our innate engager technology. We thank Martin for his many contributions to Affimed during his tenure as CSO and we wish him success in his future endeavors. Now, I'll hand it over to Florian to review our financial results.

Florian?.

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

Therefore, all numbers that I will present here in this call unless otherwise noted will be in euros. We remain well capitalized with a strong cash position.

Pro forma cash, cash equivalents and short-term deposits including the milestone payment under Genentech collaboration that Affimed received in April 2019 totaled €100.4 million or approximately $113 million as of March 31st, 2019. Cash, cash equivalents, and short-term deposits on December 31st, 2018 were €108.8 million.

Based on our current operating and budget assumptions, we anticipate that our cash, cash equivalents, and short-term deposits as of March 31st, 2019 will enable us to fund our planned clinical development and early development activities into 2021.

Net cash used in operating activities was €13.4 million for the three months ended March 31st, 2019 compared to net cash used in operating activities of €6.9 million for the three months ended March 31st, 2018.

Total revenue was €11.4 million for the three months ended March 31st, 2019 compared to €0.5 million for the three months ended March 31st, 2018. The increase in revenue is primarily attributable to the recognition of €10.6 million as revenue from the Genentech collaboration in the first quarter of 2019.

R&D expenses for the first quarter of 2019 were €8 million compared to in €6.4 million for the first quarter of 2018. The increase was primarily related to higher expenses related to clinical studies start-up activities for the AFM13 registration study in PTCL as well as early-stage development and discovery activities.

G&A expenses for the first quarter in 2019 were higher at €2.4 million compared to €2 million for the first quarter 2018. This increase was primarily related to higher personnel expenses.

Net income was €1.9 million or €0.03 per common share for the first quarter 2019 compared to a net loss of €8.2 million or €0.15 per common share for the first quarter 2018. Weighted number of common shares outstanding were 62.4 million for the quarter ended March 31st, 2019.

And with that financial overview, I'll now turn the call back over to Adi for a brief concluding remark.

Adi?.

Thank you, Florian. Thanks again everyone for joining us today. We are focused on advancing our CD16A-targeting innate cell engager product candidate as we progress through 2019 with the goals of initiating a market registration-directed study of AFM13 and entering the clinic with AFM24.

We look forward to providing additional updates in the near future. We will now open the call to take some questions. Thank you.

Operator?.

Thank you. Ladies and gentlemen, we will now begin the question-and-answer session. [Operator Instructions] Your first question comes from the line of Maurice Raycroft. Please ask your question..

Hi. Good morning, everyone, and thanks for taking my questions. First question is on AFM13. I'm just wondering if it's possible that you may provide an early look to the CD30-positive T-cell lymphoma trial before mid-2020? Since it's an open-label study I don't know if it's possible for you guys to potentially do that..

Leila, are you on the line to answer this question?.

I'm here..

Okay, very good..

Are you referring to the investigator-sponsored study?.

No, to the one that you guys are planning on starting..

I'm sorry.

Can you repeat your question again?.

No, to the Affimed study..

Can you repeat your question?.

Yes, I was just wondering if it's possible to provide an early look to that study before mid-2020 if there is reason to do so..

We're not currently anticipating doing that. I think it's important that we have a robust data set at the time of the interim analysis in order to make a determination as to the preliminary activity of the molecule..

Okay, fair enough. And then for AFM24 there's been a lot of interest in KRAS currently. I'm just wondering for that study for the initial trial if you're going to focus at all on patients with KRAS mutations..

Yes. So, that's a high area of interest and that was behind Adi's comments around the potential for the AFM24 molecule. So, absolutely that's one of the areas that we'd be very keen on testing AFM24..

Okay. So, you're going to enroll patients from these different disease settings that were mentioned and presumably some of them will have mutations and then it would just be seen if you're getting any unique activity in those patients I guess.

Is that right?.

Yes. And as you will recall that our data at AACR showed that the activity was similar in cell lines with RAS mutations versus those RAS wild type and so based on this data as well as our mechanism of action for AFM24 we would anticipate that the molecule will be effective in patients with RAS mutation as well those with RAS wild type..

Got it, okay. And just last question on AFM24.

Just wondering if you're considering combination strategies there even in their preclinical setting? Is that something you're looking at and could potentially provide a preclinical update on that at some point?.

Yes, that's a great question. So, I think we're always considering preclinical combinations and so I can't provide an update at this time on that. But certainly as a drug developer, it's always important to establish both a single-agent activity as well as a combination activity and that's something that we'll be providing updates on in the future..

Okay. Thank you. I'll hop back in the queue..

Your next question comes from the line of Jim Birchenough. Please ask your question..

Hi, guys. Thanks for hosting the call and thanks for all the detail. A few questions. I guess first just on AFM13 and the pivotal strategy. I think it was laid out shortly after the ASH Meeting.

I'm just wondering what the gating items are to starting that study? And if there's any possibility that the study initiation could be accelerated? But mainly interested in what are the gating items that check the box on just to get that study going?.

Would you like me to answer, Adi?.

Yes. Yes. Sure Leila. Just go ahead..

Okay. So we are working closely with a CRO partner to open up AFM13 Phase 2 study and related to that we filed our full study protocol with the FDA. And recall that this is a registration-directed study, with a potential for accelerated approval.

And so, with that, the FDA conducted a thorough review of this Phase 2 protocol and came back with a number of detailed technical questions. We believe we've addressed all of the FDA's questions and are currently awaiting their feedback.

So once we have a final agreement with the FDA, then we'll be able to move forward in a more robust way to get the study opened..

And just to be clear, Leila, these are technical questions that you don't expect to impact the timing of the initiation of the study? The study initiation timeline is pretty firm, is that right?.

Well, as I said, we are awaiting feedback from the FDA. We believe that we've fully answered their questions. And until they respond formally to us, I can't really comment on the precise start of the study..

Got it.

Is there a time frame for that response?.

We believe that it will be very soon. But no, it doesn't have a precise date..

Okay. Thank you. And then, Adi, just in terms of your comments around potential combinations with other NK cell therapies, I think WashU had done some work with their own NK cell therapies.

Could you maybe expand on those comments on additional -- whether there's potential for additional collaborations beyond the MD Anderson collaboration? And if that's a goal for this year, or something more we should think about for next year?.

Yes. So I made this comment more in the general perspective that other companies have taken the effort to bring NK cell-based cellular therapies forward. Some of them are just that -- we call them naked NK cells, so non-engineered NK cells that are sourced from different sources. And so, this is just one option to work with cord blood-derived cells.

And those molecules or those products have entered the clinic. On top of that we see the first engineered NK cells moving forward. Many of them now have inserted a CD16A into that, also have some other features. So there is a variety of these approaches with clinical data available soon.

And as we have pointed out, the CD16A ROCK platform gives a strong differentiation binding these cells, meaning that we have very high affinity but also the cell activity probably being able to bind to this receptor in the presence of high ITG amount.

So this is how we are looking at that, that the horizon is widening for us and gives us multiple opportunities in terms of then driving forward with AFM13 and AFM24. I would not yet want to go any further and anymore concrete on what is going to happen. But that we are still the only company with an advanced NK cell engager in clinical development.

So this is one of our big advantages..

And then maybe just for Leila on AFM24, do you anticipate initiating dosing at an active dose? Or would the initial dosing be pulled back a little bit to subtherapeutic? Just trying to get a sense of at what point we should be starting to look for data from an active dose of AFM24..

Yes. So I really can't comment on that. And I would say also that, we're also seeking some regulatory feedback on AFM24 in our overall approach. But at this point, I can't really comment on that..

Okay, great. Well, thanks for taking the questions, guys. .

Thanks a lot, Jim..

[Operator Instructions] Your next question comes from the line of Peter Lawson. Please ask your question..

Hi, Adi.

Just on the management change, will you be replacing the CSO? Or is that a role that you can kind of either fill internally or is no longer required?.

Yes. Good morning, Peter, and thanks for this question, yes? So what we currently do is, we're evaluating the needs of the organization from a scientific perspective, as well from operational needs, so that we have a robust internal pipeline, while continuing to advance our technology.

Indeed in the interim, our Chief Operating Officer, Wolfgang Fischer will oversee operations and continue to work with the team on advancing our discovery and preclinical programs. And as mentioned before, Martin continues to support us with his expertise on a consulting basis.

So short term is no quick reaction to be expected and we feel that we have already very strong people internally. So that's how far we have come..

Got you and you don't feel there's any institutional knowledge loss with Martin leaving around the ROCK platform?.

Well, I would say, every person that leaves is something where you may have some -- let me put it this way. There may be some gaps at some other places. But overall, in how we are set up, we have been working largely in teams. So our information is widely spread. And thereby we have all the capabilities and all the competencies in-house.

Again, with Wolfgang being with the company now since two years, he's heavily involved in the early discovery work already. So we see ourselves exceptionally well positioned to continue with what we have started..

Got you. Thank you.

And then, just on the ROCK platform itself, if you've seen kind of increased or decreased or about the same kind of interest from pharma partners for the potential to kind of break out to the NK cell world?.

Yes. Let me answer to this in a general fashion. We see, in general, much higher interest in innate cell engagers. So people have a much closer attention to that, since we have announced data last year at ASH, that has prompted high interest. We have single-agent efficacy.

We have very nice combination data with PD1 where we kind of doubled the complete response rates in such patient population. It's very robust, the genetic use. So for us personally the responses are very positive and there's a lot of dialogues ongoing..

Got you. And then just on the AFM13 update at ICML, what should we expect to see, I guess, number of patients? Or what kind of breakouts could we see for the mono versus the PD-L1 combination data? Anything there will be helpful..

Yeah. As I said it's an update on the data that were largely presented at ASH. So as compared to ASH we've had six months data. Now we can present the full 12 months' data as an update. And there is additional for the Columbia study. So the AFM13 mono study in T-cell there is additional insights given on the translational aspects of this study.

As you may recall we have not just investigated the systemic effect of our drug but also have taken serial biopsies in order to understand NK cell and macrophage activation both peripheral and within the tumor itself. So such data will be presented..

Got you. And then just finally on AFM24, so the EGFR targeting molecule.

The indications -- are there particular indications you're thinking of initially? Or could this be a tissue agnostic approach? And it sounds like you could have, I don't know if it was like an actual cohort for KRAS mutations or that would just be a general inclusion criteria? Thank you..

Leila, do you want to take a shot on this question?.

Yeah. So I'll say that firstly the final protocol is still under review internally with our investigator partners, our thought leaders and with the health authorities. So it's still under active discussion. That being said, I think it's really important that we benchmark the activity of our engager versus other EGFR-directed therapies.

And so what we're thinking is to focus in on populations where we understand well how the other EGFR targeted agents would work or not work and then be able to demonstrate fairly quickly that AFM24 is differentiated from these other source of approaches.

So what comes to mind, obviously, then would be non-small cell lung cancer and colorectal cancer in particular. But we're considering other indications as well..

Great. Thank you so much..

Thank you, Peter..

Your next question comes from the line of Daina Graybosch. Please ask your question..

Thank you for the questions. The first one back on the AFM13 potential registration study.

As you await the FDA's feedback are you going forward at risk with some of the other trial planning activities like identifying the site, finalizing your staff et cetera? Or in other words, how fast can you start after you get that feedback from the FDA?.

Thanks, Daina. So that's so exactly what we are doing. We are doing all of the preparation activities that we can prior to gaining that final FDA feedback, so that we can minimize the time from finalization of the protocol to study start-up..

Great. And one more on that.

Did you also -- are you're also getting feedback from the EMA?.

With respect to AFM13 study? Phase 2 study?.

Exactly, the….

We have not heard back specifically from the EMA..

Okay. And then another couple competitive questions. The first one is a couple of people have already mentioned the excitement around the KRAS mutation inhibitors from Amgen and Mirati, a slightly different question on that.

Do you have any pre-clinical data on how AFM24 would compare to an inhibitor going after a targeted mutation like one of these?.

So we have not generated comparative data to that degree. We know that AFM24 is cytotoxic independent of these mutational status and we have done some comparison with cetuximab but we have not compared it to any of the other small molecule compounds out there..

Okay. And then one last question, you mentioned some of the new engineered NK cells entering the clinic to engineer in a high affinity CD16A.

A two-part question, how do you think you would compare combining with let's say un-engineered cord blood NK cells versus those cells combining with something like cetuximab? Can they achieve the same efficacy improvement that you achieved by basically putting the affinity on the cell? And then the second part is, if you combine your engagers with such a cell, do you think you can get even more efficacy with modifications on both ends?.

Yes. So again some of my answers is data-driven some are speculative in here on how we see the technologies. But the first and most important, when you look at the true affinities of IgGs versus our process we have a huge affinity advantage of about 1000-fold and higher. So we have much stronger binding.

And secondly we know that the circulation is quite full with circulating IgG that all have the same binding domains that compete for natural killer cells. So that gives us a much higher chance of -- much higher probability of success in order to bind the natural killer cells and then redirect them.

When we pre-clinically are incubating natural killer cells with our engagers versus an antibody and then you have to do some washing steps in between, we know that IgGs do not wipe these washing steps. So they will be completely washed off such in case elsewhere our approach allows a full coverage and is just much stronger.

So if you take a washed cell and then use that for therapeutic models in vivo models we see very high efficacy of these pre-incubated cells that we cannot achieve otherwise with antibodies. So that means that we are indeed injecting already an in situ CAR NK.

When you then have to do this by a separate fashion, so if you inject your NK cell and your antibody into a patient as I say you are then -- you have to overcome this huge hurdle of internally -- of the internal IgG levels. This is again another advantage.

So this is why we think that our approach can have much higher and much deeper efficacy as compared to what's out there currently.

Did that answer your question?.

It does and then I guess the second question was, if you combined with one of these engineered NK cells, how much efficacy improvement do you think you could get versus combining let's say the cord blood unengineered NK cell?.

Yeah, it's all dependent on the CD16A expression that is on the let's say the non-engineered cell that sometimes varies in a certain degree of how we know that there is a high degree of CD16A already present. So I would not speculate yet if the one or the other approach is the better approach. We don't have yet generated data.

But the point that I wanted to make is, we're agnostic about that. So I think with the cord blood derived we have a very state-of-the-art product that's clinically tested. We know that it has a very good safety profile. So we felt this is the right thing to do and go with this first because there is abundant amount of clinical data available.

All the other approaches now have to prove its safety in the first place. But again, when they then have established the safety is the key question what are they going to combine with because, we know that these cells that are not targeted, NK cells have still challenges of identifying the malignant cells.

And that's where innate cell engagers such as our molecules can basically be the bridge in this context. So we see chances to -- we see good chances to be successful with the cord blood-derived cells. But we will also obviously carefully follow what the -- how the profiles of the other molecules are.

So what I'm telling you is just there is more in the -- more available to patients and we are very unique with our innate cell engagers and we have a very unique positioning and differentiation..

Great. Thank you. That’s all the questions I have..

Your next question comes from the line of Yale Jen. Please ask your question..

Thanks a lot for taking the questions. Probably I'll start with some housekeeping ones for modeling purpose. First of all, is that you have a milestone payment from Genentech in the last quarter -- the fourth quarter of last year as well as first quarter this year.

I anticipate this is to be lumpy, but what should we sort of think about in terms of topline perspective for remaining of the year?.

Hi, it's Florian. Thanks for question. So I think the first topic is that we have received one milestone payment and this is the -- since we signed the agreement. So we received the up-front payment last year and this is now -- this was the first milestone payment.

We cannot comment on the likelihood of receiving other milestone payments and therefore, we also don't have it basically in our cash assumptions or in the budget. The milestone payment was a preclinical milestone and that was related to one of the projects..

Okay. Great. That's very helpful. And then maybe again a housekeeping question which is the first quarter this year, the R&D expense and SG&A was materially lower than the prior quarters.

Again for modeling purpose, should we consider this to be something annualized based on the first quarter figures? Or that will be increased much more substantially going forward?.

So I would -- we don't usually -- so the way we model it basically bound to content and not so much on periodic effects. So therefore, I would rather -- even being cautious I would rather see this as in an increasing level given all the activities that are currently ongoing in the company..

Okay. Great. And then maybe just last follow-up question on two of the pipeline products. First, in AFM13, in terms of the adaptive NK cell study, what the MD Anderson -- in the press release, it's said that it is planned.

Could you give us maybe a little bit of color in terms of whether this program may start second half of this year? Or there's more -- what more details to that?.

Leila, can you take that question? Yes, thank you, Leila..

I was checking at the question. So just to remind everyone this is an investigator-sponsored study under the control of MD Anderson. We've had multiple discussions with MD Anderson and they appear to be working very diligently to start the study as soon as possible. We can't therefore communicate the precise start of the study.

But as soon as the study has started, we will be certain to inform you of that..

And maybe the last question for the AFM24 in terms of the Phase I study.

Would you also explore the possibility even at the Phase I stage for EGFR sort of resistant patients to explore the possibility of the -- the potential of the AFM24?.

Yes. Absolutely. I think it's important that those sorts of patients are included in the clinical study early on..

Okay. Great. Thanks a lot. Appreciate it..

Your next question comes from the line of Jim Birchenough again. Please ask your question..

Yes. Hi guys. Just a couple follow-ups.

Just first, Adi, if could you comment on the potential role or need for cytokine support for innate cell-targeted therapies IL-15 specifically? And maybe comment on where we're at with the Nektar collaboration?.

Yes. Thanks again. So let me just first talk a little bit about the Nektar. So the Nektar aimed at combining our innate cell engagers with IL-15.

And if you may recall, we have already published some data on other IL-15 molecules not the Nektar derived one, but some different one and have shown synergy that we can see a stronger cytotoxic effect to a higher degree of lysis when IL-15 is present and that rather relates to a proliferation of the Natural Killer cells.

IL-15 effects have been described in patients also to enhance immune cell function mostly by increasing the number of NK cells. So that also fits the picture that it's probably a very valid idea a good rationale to combine innate cell engagers with IL-2 or IL-15. So it probably could take either of those two.

I cannot comment further on the Nektar collaboration. So we have explored the molecules in some of our models. We are basically wrapping up and thereby have concluded the collaboration with Nektar at that stage. Now you asked me for a general role of these molecules in the context of combining it with cellular therapies.

So there are different approaches out there regarding IL-15. Some have expressed as a part of their engineering of Natural Killer cells, so that the Natural Killer cells can have a longer persistence. And it's definitely helpful, but I believe -- we believe this is particularly helpful for those that are just working with cellular products.

As you may recall these are very often allogeneic off-the-shelf products that may have just a very short persistence within the patient. So there is a limit on how often you can give it and how long the effect may be there. It's a little bit different when you think about the approach what we could do with innate cell engagers.

So we have on the one side the option to combine innate cell engagers with these cellular products, but we also can continue dosing just with our innate cell engagers and thereby relying on patients' own Natural Killer cells and macrophages.

So this is a very distinct differentiation, and obviously, we are looking at what's happening with IL-15, but we may not consider this as the key component to be added in. So just a combination with a large number of Natural Killer cells with our innate cell engagers and then single dosing of -- continued dosing of innate cell engagers.

This is how we think and could be a very differentiating approach..

And then maybe just one final question and might actually be for Florian, but there's been considerable investment in AFM11 and the T cell engager part of the business.

And just wondering if there's any way to monetize that know-how in any of those assets even earlier-stage assets if you think that's a potential source of non-dilutive capital perhaps?.

That's what we are currently evaluating. So our goal has been with the FDA to lift the hold. We've had an ongoing dialogue. So there is an opportunity to resubmit drug's data. Just Affimed has decided that we feel our resources are dedicated to ongoing programs and new programs.

Yes, so the way how it is at the moment, it leaves some options open for AFM11. There may be an opportunity that we can monetize, but it's not in our -- it's not our key strategy and key focus in order to have any priorities on that. So we are looking at inbound interest and then we check on what kind of interest there is..

Terrific. Well, thanks for taking the follow-ups..

Thank you..

There are no further questions at this time. Dr. Hoess, please go ahead..

Thanks a lot for listening to our earnings call today. Highly appreciate it for your attention and the many questions we were receiving and I wish you all a very nice day. Thank you. Bye-bye..