Anca Alexandru – Head of Communications Adi Hoess – Chief Executive Officer Anne Kerber – Interim Chief Medical Officer Florian Fischer – Chief Financial Officer.

Michael Schmidt – Leerink Do Kim – BMO Capital Markets Maury Raycroft – Jefferies Yale Jen – Laidlaw Nick Abbot – Wells Fargo.

Good day, ladies and gentlemen and welcome to the Affimed First Quarter 2017 Financial Results and Corporate Update Conference Call. At this time, I would like to turn the conference over to Anca Alexandru. Please go ahead..

Thank you. I would like to welcome you to our investor and analyst call on the results for the first quarter of 2017. Before we start, please note that this call and the Q&A session contains forward-looking statements, including statements regarding our future financial condition, business strategy, and our plans and objectives for future operations.

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 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.

Thank you for your understanding. I will now hand the call over to our CEO, Adi Hoess, who will provide the corporate update..

Thank you, Anca. With me on the call today is Florian Fischer, CFO, who will present the financial update and interim CMO, Anne Kerber, who will provide an overview on our clinical program. We can go to Slide 3. Affimed engineers targeted immunotherapies, seeking to cure patients by harnessing the power of innate and adaptive immunity.

Our approach is to eliminate tumor cells by recruiting NK-cells or Natural Killer-cells or T-cells. We have clinical and pre-clinical assets in our pipeline of next generation immune cell engagers is based on tetravalent bi and trispecific antibody formats.

We are an industry leader in NK-cell engagement and our lead product candidate AFM13 is to our knowledge, the most advanced NK-cell engager in clinical development.

We also have a well-differentiated T-cell based approach which includes our clinical candidate AFM11 and I’ll provide an update on these clinical programs as well as our pre-clinical programs later. We have ongoing partnerships with industry, academia, and advocacy groups.

We employ about 75 full time people with our headquarter located in Heidelberg, Germany, and affiliate offices in the U.S., that is Affimed Inc., and our subsidiary AbCheck in Plzeň, in the Czech Republic. Slide 4.

We have an unencumbered clinical and pre-clinical pipeline of NK and T-cell engagers, with our NK-cell engagers being developed in hematological diseases and solid tumors. Based on our NK-cell platform, we have one clinical and two pre-clinical programs in development; and based on our T-cell platform, we have one program in clinical development.

Amphivena, a company of which we own 23% as recently entered clinical development for a bispecific antibody derived from our technology platform. Our first quarter update include both financial and program process.

As previously communicated, we have completed a follow-on offering in the first quarter, expanding our runway at least until the end of 2018.

On the program in the Phase 2 immunotherapy trial for AFM13 sponsored by the German Hodgkin Study Group, we had previously announced a study amendment, with the study that will now recruit patients pre-treated with both brentuximab vedotin and anti-PD1.

In the meantime, we have analyzed the outcome in patients in the original study population, it is treated with brentuximab vedotin, but naïve to anti-PD1, and we saw two partial responses out of seven patients. In the Phase 1b combination study with anti-PD1, we have progressed to the highest dose level.

In January 2017, we entered into a collaboration with the University of Texas, MD Anderson Cancer Center to evaluate our tetravalent bispecific immune cell engager technology in combination with MD Anderson’s natural killer cell product.

In April, we had oral and three posters at AACR on our NK-cell engager AFM13, AFM24 and AFM26, as well as on our MHC peptide-targeting discovery program.

In our T-cell engager programs we opened additional sites to accelerate recruitment for AFM11 and Amphivena initiated treating AML patient with AMV564, a bispecific tetravalent, CD33/CD3 antibody derived from Affimed’s technology platform.

In order to broaden the target base for T-cell engager, we are generating bispecific key and NK-cell engagers against MHC-peptide complexes, and presented data on the specific killing of tumor cell lines carrying the specific complex only, but not of a large number of control cell lines. Slide 6.

Before I provide an update on our clinical and pre-clinical pipeline, I would like to explain the main characteristics of our technology. As compared to most competitors, Affimed is using a unique approach with its tetravalent bispecific antibody.

The bivalent binding to two receptors and the two different cells enables high affinity binding through the avidity effect, which is advantageous to obtain and maintain high specificity. This is highly important to achieve a good safety profile. Furthermore, our platform allows multi-specificity and a Tailored PK.

We believe that NK-cells are becoming a cornerstone of cancer immunotherapy and we are excited to be pioneering this development. There are a number of reasons why NK-cell based approaches are very attractive and one of the reasons is that that seems to be a positive correlation between NK-cell infiltration and clinically outcome in patients.

In this context it has been described that a low cytotoxicity is associated with high incident of cancer. Also NK-cells are similarly potent compared to T-cells in terms of cytolytic potential, however they differ in their biology.

In addition, recent clinical data showed improved antitumor responses of ex vivo expanded and activated NK-cell population. Today it seems like NK-cell based approach have the strong advantage of having a well manageable favorable safety profile.

We believe that the safety profile of NK-cell engagers is highly differentiated from T-cell engagement and may confirm much lower toxicity. This will be a potentially better treatment choice, for example, for elderly patients in hematology and oncology.

For example, in multiple myeloma or AML, and could further position the NK-cell platform as a leading platform in solid tumor indication. Also the lack of ability to recognize malignant cells can be overcome by either manipulated NK-cells or even simpler with our NK-cells engager.

I comment theme in all different cancer types is the ability of the tumor cell to evade recognition by the immune system and specifically NK-cells. Normally NK-cells are capable of killing foreign or aberrant cells, but tumor cells have acquired mechanisms to escape the so-called immune surveillance.

As a result, such NK-cells cannot recognize tumor cells as foreign or aberrant and therefore cannot fight them. Our platform has the potential to overcome these limitations by disabling the tumors’ evasion mechanisms.

Our expertise and leadership in natural killer cell-based approaches is one of our key assets and we believe that targeting CD16A, a dominant activating receptor on innate immune cells is the key for efficient recruitment of and killing by NK-cell and macrophages.

Our antibodies bind immune cells through CD16A with high affinity and specificity inducing NK-cell activation, which triggers an integrated immune response mediated by both innate and adaptive immune cells.

We’ve demonstrated for several of our antibodies that our NK-cell platform is strongly differentiated from regular IgGs or Fc-enhanced IgG antibodies; for example, regarding competition with speculating IgG. I will hand the call over to our acting CMO, Anne Kerber, who will provide an overview on our clinical trial..

Thank you, Adi. Let’s move to Slide number 9 then. Our lead product candidate, the CD30/CD16A-specific NK-cell engager AFM13 is a first-in-class antibody suitable for mono and combination therapy. It has demonstrated safety and clinical activity in heavily pretreated Hodgkin Lymphoma patients in a Phase I study.

In this Phase 1 study tumor shrinkage and partial responses are observed in patients treated with full weekly doses of at least 1.5 mg/kg AFM13. In 62% patients which was eight out of 13 patients we observe tumor shrinkage and 23% of patients we see total of three out of 13 experience partial responses.

Based on these data together with the German Hodgkin Study Group or GHSG we initiated an investigated sponsored Phase 2a trial for AFM13 in relapsed or refractory Hodgkin Lymphoma in the second quarter of 2016.

However, as communicated in the past, recruitment into the study became quite challenging because the treatment landscape for Hodgkin Lymphoma has evolved rapidly. More patients received brentuximab vedotin marketed under the name Adcetris.

And in addition, an increasing number of relapsed or refractory patients are being treated with recently approved anti-PD1 antibodies.

Accordingly, as previously announced, the study protocol for the investigator sponsor Phase 2a monotherapy trial of AFM13 in Hodgkin Lymphoma had been amended by the study’s sponsor, the German Hodgkin Study Group, to ensure the recruitment of a homogeneous patient population.

The study will now recruit patients pre-treated with both brentuximab vedotin and anti-PD1 antibody. In addition, different dosing regimens are being investigated to provide improved exposure and convenience in these very heavily pre-treated patients.

I’d like to share with you some preliminary data from patients enrolled into the trial under the original study protocol. Recall that the patients at failed prior standard treatments including brentuximab vedotin and were anti-PD-1-naive.

We observed partial responses in both arms of the study and even though we are talking about small patient number here. This is exciting for us because this for the first time suggests that AFM13 is active as a single agent in this heavily pre-treated group of patients and in particular that AFM13 is active for brentuximab vedotin.

In detail, two out of seven patients in this sub group experienced partial responses. We continue to anticipate providing an update on the study in the second half of 2017, where the study is expected to begin recruiting under the new design in the first half of 2017.

Full data from the ongoing study will be presented upon its anticipated completion in 2019 and it will be up to the study sponsor the German Hodgkin Study Group to determine the timing of this update. Slide number 10.

We are also developing AFM13 as a combination therapy, pre-clinical affinity has been demonstrated in combination of anti-PD-1 in vivo in the PDX model and this synergy might be attributable to induce crosstalk between innate and adaptive immunity illustrating and integrated immune response.

This has been the basis of our Phase 1b trial in relapsed or refractory Hodgkin Lymphoma in combination with Merck’s Keytruda, which we initiated in May 2016. No dose limiting toxicity is for the combinations were observed in the first and second dose cohorts of the study.

Data read-out is ongoing in the treated cohort and we anticipate providing an update on the study in the second half of 2017. Additional opportunities for our NK-cell engagers include combinations with adoptive NK-cell transfer, which we are investigating with our partner MD Anderson.

Affimed will fund research and development expenses for this collaboration and the agreement includes a provision for the potential expansion of the partnership. Initially we planned to investigate AFM13 with MD Anderson’s NK-cell product in Hodgkin Lymphoma.

Pre-clinical research activities are on track and these intended to be followed by a Phase 1 clinical trial. Proof of concept for this combination in Hodgkin Lymphoma would also pave the way for combination of other pipeline product in combination with NK-cell. One example is AFM26.

Affimed holds an option to exclusive worldwide rights to develop and commercialize any product developed under the collaboration. A further opportunity is the combination of our antibodies with cytokines.

In recent pre-clinical studies, we have demonstrated that AFM13 induced upregulation of specific interleukin receptors on NK-cells in a target-dependent manner and sensitized NK-cells for IL-2 or IL-15-mediated expansion. And at AACR in April we provided additional insights into the molecular characteristics and function of our NK-cell engager.

The data highlighted AFM13’s potential to therapeutically reactivate NK-cells that are dysregulated in cancer and support the strategy of clinically combining our NK-cell engagers with cytokines to potentially achieve deeper clinical responses. We have recently submitted a manuscript on data for publication.

Slide 11, our efforts in T-cell engagement has led to the development of differentiated product as well as a novel platform. AFM11 targeting CD19 and CD3 has designed to address the high unmet need in Diffuse Large B-Cell Lymphoma and Mantle Cell Lymphoma that remains despite recent CAR-T data.

It addresses limitations of other bispecific such as the need for CIV administration over period as long as four week or moderated efficacy and has demonstrated higher potency at low T-cell, high targets on numbers as compared to CD19/CD3 binds.

We have two Phase 1 dose escalation trials ongoing for AFM11, one in patients with relapsed and refractory acute lymphocytic leukemia and one in non-Hodgkin lymphoma, both trials are ongoing and recruiting.

Recall that we have previously amended these trials to address the challenges in recruitment in these trials, which had rising among other factors due to the early availability and reimbursement in certain countries.

Moving the trials to other countries has considerably improved recruitment fees in particular in our ALL trial precise in Czech Republic, Poland, Russia, and Israel are up in running. We are adding size on an ongoing basis to further accelerate recruitment. We expect to provide a progress update on both trials in our second quarter earnings call.

In July, 2016, an IND for the bispecific CD33/CD3 T-cell engager, AMV564, a molecule developed from Affimed’s technology platform became effective. AMV564 is being developed by Amphivena Therapeutics Inc. to address the high unmet need in AML.

AMV564 is well-differentiated with its potent and selective cytotoxic activity and robust tumor growth inhibition. Amphivena has initiated approach in human Phase 1 dose escalation and expansion trial of AMV564 in patients with relapsed or refractory acute myeloid leukemia.

We own 23% of Amphivena and has participated in their recent Series A-extension financing. We have successfully developed another technology platform to open up that therapeutic target space. The platform is designed to generate antibodies targeting disease specific MHC-peptide complex.

Access to these intracellular target is highly attractive for both T and NK-cell recruitment and we have generated and preclinically investigated T-cell engager specifically binding such MHC-peptide complex. Together with our collaboration partner Immatics and our subsidiary AbCheck, we presented data at AACR on this novel platform.

I will now turn the call back over to Adi for an update on our preclinical programs.

Adi?.

Thanks, Anne. We are now in Slide 12. We are developing a first-in-class NK-cell engager addressing the unmet need to effectively treat EGFR expressing solid tumors such as lung, head and neck or colon cancers. AFM24 is designed to improve both efficacy and safety of current therapeutic monoclonal antibodies.

It is well differentiated from cetuximab with more potent cytotoxicity in vitro and in vivo, as shown in our slide including Ras-mutant cell lines. Through its novel mechanism of action and safety profile, it has the potential to overcome intrinsic or acquired resistance, which is described indeed for many patients.

Data presented at AACR showcase AFM24’s novel mechanism of action offering higher efficacy and an improved safety profile as compared to current EGF Receptor targeting marketed agents.

In particular, in vivo data showed an excellent safety profile in toxicity studies in cynomolgus monkeys, with single intravenous administration being well-tolerated up to the highest dose level of 93.75 mg/kg. In safety profile offers the rational for combination of AFM24 with PD-1/PD-L1 antibodies in solid tumor indication.

We planned to present further data on AFM24 at the EACR-AACR-SIC Special Conference in Florence, Italy, in June 2017. On Slide 13 is the AFM26, which we’re developing to treat multiple myeloma, the second most common hematologic cancer. AFM26 is a first-in-class tetravalent bispecific antibody targeting BCMA/CD16A.

MM is characterized by high serum levels of monoclonal immunoglobulin, so-called M-protein and most patients eventually relapse with and/or become refractory to current available treatment. AFM26 introduces a novel mode of action conferring high-affinity to both target and NK-cells, which leads to a prolonged cell retention.

AFM26 shows high cytotoxic activity towards BCMA-expressing myeloma cell lines, and importantly it NK-cell binding appears to be virtually unaffected by the presence of high levels of IgG.

Based on these characteristics, AFM26 might potentially be positioned in first line as combination with adoptive NK-cell transfer during stem cell transplantation or in salvage setting. It is potentially safer than T-cell-based approaches which could allow for faster development timelines.

In AACR, in April, we present a data which underscored that compared to a T-cell engager. AFM26 is similarly potent, but shows a reduced cytokine release pattern. This points to an improved safety profile, making AFM26 uniquely suited to engage NK-cells in multiple myeloma.

We plan to present further data on our BCMA-targeting antibodies at the upcoming ASCO Annual Meeting in Chicago, and at the same – at different conference in Florence, Italy, both of which will be in June 2017. I will now hand over the call to Florian Fischer, who will provide further details on the financial figure..

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

Therefore, all financial numbers that I will present here in this call unless otherwise noted will be in euro. Any numbers referring to Q1 2017 and Q1 2016 are unaudited. Cash and cash equivalents and financial assets totaled €53.7 million as of March 31, 2017 compared to €44.9 million as of December 31, 2016.

The increase was primarily attributable to the net proceeds of €16.4 million from the public offering. Net cash used in operating activities was €7.2 million for the first quarter of 2017 compared to €8.5 million for the first quarter of 2016.

The slight decrease was related to lower cash expenditure for research and development in connection with our development and collaboration programs. Affimed expect to have cash to fund our operations at least until the end of 2018.

This provides runway for the plan development of our clinical programs as well as for the further discovery and early development activity. Revenue for the first quarter of 2017 was €0.4 million compared to €1.9 million for the first quarter of 2016.

Revenue in the first quarter of 2017 was derived from Affimed’s collaboration with LLS and AbCheck service revenue, while revenue in the first quarter of 2016 related predominantly to the collaboration with Amphivena.

In the first quarter of 2017, Affimed funded Amphivena with €0.6 million, which was offset against consideration under the Amphivena agreement of €0.5 million. Without this effect revenue would have been €0.9 million for the first quarter 2017.

R&D expenses for the first quarter of 2017 were €5.4 million, compared to €7.1 million for the first quarter of 2016. The decrease was primarily related to lower expenses for AFM13, preclinical programs and infrastructure.

G&A expenses for the first quarter of 2017 were nearly unchanged with €2.2 million compared to €2.1 million for the first quarter of 2016. Net loss for the first quarter of 2017 was €7.8 million, or €0.19 per common share, compared to a net loss of €8.5 million, or €0.25 per common share, for the first quarter of 2016.

The decrease in net loss was primarily related to lower spending on R&D for AFM13, preclinical programs and infrastructure. In addition, the result was affected by lower revenue and lower finance costs. I will now turn the call back over to Adi for summary of our two clinical programs and our pipeline.

Adi?.

Thanks a lot, Florian. As shown now on Slide 16, we have an unencumbered clinical and preclinical pipeline of NK and T-cell engagers, with our NK-cell engagers being developed in hematologic diseases and solid tumors.

Based on our NK-cell platform, we have one clinical and two preclinical programs in development and based on our T-cell platform, we have one program in clinical development and for another T-cell based program Amphivena, a company of which we own 23% as recently enter clinical development for an antibody derived from our platform.

Our NK-cell platform comprises three programs, the lead drug AFM13 is currently investigated in two clinical trials and we have developed further options to broaden its application. In addition, we have two more drugs, AFM24 and AFM26 in preclinical development.

Regarding T-cell engagement, we’re focusing our efforts on AFM11, which is being investigated in two clinical studies. We have further developed a novel platform that enables the targeting of MHC-peptide complex. We indeed expect to generate significant [indiscernible] throughout 2017, providing updates on all our clinical and preclinical programs.

Our strategy is to maximize the value in our pipeline and platform. We are leveraging our lead product AFM13 plus CD30-positive lymphoma initially focusing on the Hodgkin lymphoma salvages setting enabling a fast development path and it would allow the establishment of a cost efficient M&A structure.

In addition, we believe investigating AFM13 both as monotherapy and in combination with Keytruda reduces its development risk. Overall our preclinical and clinical strategy is designed to broaden the scientific leadership of our NK-cell platform with CD16A as proprietary target.

We are expanding the preclinical and clinical activities of our tetravalent bispecific NK-cell engager platform in solid tumor with our preclinical candidate AFM24 and in hematologic diseases, where we intend to leverage additional opportunities for AFM13 and AFM26, for example in combination with adoptive NK-cells.

We also developed T-cell engagers and our lead T-cell engager AFM11 is being investigated in two ongoing ALL and NHL trial. AMV564, T-cell engager derived from our technology platform is being developed by Amphivena to treat AML and has recently entered the clinic. Thank you very much for your interest and call is now open for questions..

Thank you. [Operator Instructions] We shall take our first question from Michael Schmidt of Leerink. Your line is open. Please go ahead..

Hey, thanks for taking my questions. I had a question regarding the AFM13 monotherapy Phase 2a study. So I think if I heard you correctly, you said, you saw two responses in seven patients treated to date. But you’ve talked about responses in both arms of the trial.

Can you just remind us of the study design, what are the differences in the various arms that have been run and talk a little bit more about the treatment history of those patients were they post-transplant, were transplant ineligible any more color there would be helpful. Thanks..

Sure. So the study – the initial study design was setup in a way that we have two different treatment arms. One is a 7 mg/kg dose given once weekly and the other one is three times 1.5 mg/kg per week. That’s the two different dosing arms and as said, we’ve seen responses in both arms.

The treatment history is such that those seven patients that we reported on to date all have been pretreated with brentuximab vedotin unless they have failed previous standard of treatment and that all of these seven patients were a checkpoint inhibitor naive..

Okay, thanks. And then, I think you said, your update regarding the AFM11 program in the first half of this year which I guess in a few weeks. So my question is, what your expectations would be regarding this update? Will you present some data from these patients in non-Hodgkin Lymphoma and ALL? And are your expectations before that? Thanks..

So as we have previously communicated, we have some issues with the recruitment of patients into these trials. We have taken a lot of measures on that. And dose escalation is on there in currently.

What we intend to do is to give you an update in our next earnings call which we planned in the second quarter earnings call and then give you a status update on where we are in this dose escalation..

Okay. Thank you very much..

We shall take our next question from Do Kim from BMO Capital Markets. Your line is open. Please go ahead..

Hi. Good morning. Thank you for taking my question.

For the two partial responses that you saw in the monotherapy study of AFM13, was the responses measured under the traditional IWG criteria or were they early adaptive immune-related response criteria?.

No, it was measured according to adjustment 2007 [ph]. So it was not adapted according to immune-related response criteria, not according to IWG, it’s based on adjustment 2007 [ph]..

Okay.

And how long did it take to be a responsive? And do you have any sense about how durable these responses were?.

We do not yet have a sense how durable these responses are because the follow-up is not long enough. And our response assessment – our first response assessment are approximately three months. And that’s when these responses were documented..

I see.

And from a safety standpoint, did one of the two dosing regiments looked better than the other?.

Right now we haven’t seen any obvious differences, but the data analysis is of course ongoing and this is a nice – we don’t have a full picture in terms of the exact adverse event panel form. But from what we know, there is no significant difference..

I see.

And does the vascular expect to all these patients onto their next treatment line and will you get the data of whether or not they respond to their next treatment line? Just trying to understand whether if they’re treated with a PD-1 inhibitor after AFM13; would you expect to see a stable level of efficacy that we’re partially seeing at PD-1 or is there some possibility that AFM13 would reduce the response?.

I mean that of course hypothetical, but based on the mechanism of action I wouldn’t think that there would be a different response to a checkpoint inhibitor, but of course we don’t have data on that.

The only extrapolation that we can make is that also after brentuximab vedotin which of course has a different mechanism of action, but these also try to take us through the antigen and the response is through the checkpoint inhibitor look quite impressive.

And I would say, as of today, I wouldn’t have any concerns that the activity after AFM13 would be impaired..

Great. Thank you for taking my question..

You’re welcome..

We shall take our next question from Maury Raycroft from Jefferies. Your line is open. Please go ahead..

Hi. Congrats on the progress and thanks for taking my question. I was just wondering for the other five out of seven patients if there were any stable diseases observed; and also if there’s any perspective on biomarkers to such as peripheral NK-cell or if there’s an impact on PD-1/PD-L1 expression levels..

Yes, we do actually analyze NK-cell sub population and also NK-cell function in this study. But also this is currently ongoing and we don’t have a full data set yet, and we’ll also be only on a subset of patients. So I cannot give you any results on potential biomarkers in that study yet at this point in time.

And the other five patients, I cannot say right now, I would need to get back to the German Hodgkin Study Group to get more data. In fact, they are the response of the study, so they will have a full data set.

The only thing I can conform is that these two partial responses are actually partial responses that have been conformed by an independent panel as a German Hodgkin Study Group. So it’s not local assessments only, but it’s confirmed by central rates..

Okay. And then also for the monotherapy amendments that are being made, you mentioned that it could improve exposure and also convenience too. I was just wondering if you can elaborate on this.

And you anticipate that the doses will compare to the Phase 1 study and how will convenience change?.

Yes. I mean, I think for that question we have to keep in mind that because we are not the sponsor of that study. We cannot go in detail on these questions. We have to align with the German Hodgkin Study Group so that we can provide our guidance with what they advices at this time in the discussion with us.

So I think on that one we will not be able to provide more details right now..

We’re in additional learning is that that dosing regiments that we are developing indeed are quite innovative; indeed, it represents a very specific know-how. So that means that you can develop a competitive advantage by certain dosing regimes.

And that’s why we at the moment at least do not want to share any details on how we are continuously developing our NK-cell and T-cell engager. But again just to reemphasize that, we’re learning a lot from these studies in order how to optimize the administration, and it’s something that we consider proprietary..

Got it.

And for the MD Anderson collaboration, I’m just clarifying that, are those allogeneic or autologous NK-cells that are being used?.

That’s cord blood derived. So in essence, it’s an allogeneic. If you want to….

Yes. They have that in the clinic already in multiple myeloma, and in AML, and had shown that this approach appears to be safe with lactotroph versus host disease. And because they’re fairly in the forefront with there’s – this platform we’ve teamed up with them and are indeed quite excited that we can now develop the combination.

And as we’ve said before, AFM13, our mind is the starting point. It will hopefully provide a proof of concept for such of combination, but clearly we are in between that we can broaden that to other hematologic diseases that we have already mentioned our AFM26 molecule that we’re developing multiple myeloma.

So that’s another setting we’re looking forward to work MD Anderson..

Great. Okay. Thank you for taking my question..

We shall take our next question from Yale Jen from Laidlaw. Your line is open. Please go ahead..

Good morning and thanks for taking the questions. I just want to go on two patients that have partial response.

Are they – one of each from the dosing group or both from the same dosing group? And which one is that?.

One of each..

Okay. And second question is that you’ve talked – I mean, talked about NK transfer a combo, and eventually move to clinic.

Is there a timeline you can think of, would that be something in 2018 or how should we think about that particular implementation there?.

We are currently doing pre-clinical work together with MD Anderson which is on track, but we haven’t communicated yet any timelines on where we would start a clinical development program..

Okay. And the last question I have is that you mentioned that there’s a benefit by having IO-2 and IO-15 that can stimulate that activity overall. So was there any thoughts about what specific sort of clinical implementation of that specific studying at least your contemplating and then if so – is there any timeline we can think about? And thanks..

To your concrete question, I need to be a little bit open ended here. So what we have been doing is that we have been screening the field to have molecules in clinical development that either would on IL-2 or IL-15 in cytokines molecule.

And so these discussion are ongoing and indeed currently, we can do this in fact things where we would use AFM13 through one of the potential combinations would be applied again to Hodgkin lymphoma or CD30-positive lymphoma patient, but we also intending to test that in preclinical safety if possible and then with our two preclinical drugs the AFM24 and AFM26.

So this is a little bit early yet to give you any concrete outlook on how that’s going to happen. But discussions are underway with respective players in the field..

Maybe just curious – if just where crudely adding for example IL-2 in different doses would that alone could have any impact or again too early to think about in the human cancer setting..

On preclinical data suggest that this might be an approaches works like to pursue, however I would say with conclusion into clinical activity, I would be careful at this point in time. I think that there is not enough data there yet to draw to be – to draw a final conclusion or potential clinical activity in combination..

Okay. Thank you very much..

[Operator Instructions] We shall take our next question from Jim Birchenough from Wells Fargo. Your line is open. Please go ahead..

Good morning, it’s Nick on for Jim this morning in. Congratulations on clearly validating this AFM13 active as a single agent and refractory Hodgkin Lymphoma. It’s been a long journey for you. So I’m sure you’re delighted with that data. And I know obviously you don’t have all of the data or that I’m sure you’d like it’s with the German Hodgkin folks.

But do you know anything about the responses to brentuximab in your two responding patient had, I mean had they been – did they have a good response to brentuximab or were they primary failure. And then I have a follow-up..

We have a commitment from the German Hodgkin Study Group that they will provide us with more details on the pretreatment of patients with that – we don’t have that yet. But maybe we will be open to answer that question in the next call if that should be possible..

Okay. Obviously, they are very powerful organizations.

So do you get a sense that now they have this data with the revised protocol that you would expect to be in it increased in recruitment from centers to a part of that group? And then in addition the dose modifications that you’re making in that study, will they be reflected in all the ongoing studies and particularly your PD-1 combination study? Thank you..

No, that regimen will be first explored in the Hodgkin Lymphoma study with that we’re running with the German Hodgkin Study Group.

We do expect that recruitment will pursue continuously and well, specifically as we had at the beginning a slow starting Phase mainly due to operational delays and the opening sites and of course we’re on beyond that point right now. So that sites are up and running and we hope that we can implement that new dosing arm study quickly..

Okay. Good, excellent. And then on the MD Anderson collaboration, I know you just mentioned that you’re looking prior to IL-15 like molecule obviously MD Anderson that published on intend IL-15. Is that – can you access that technology as part of your collaboration..

Good question, Nick. Let’s put it this way. I mean we have signed the contract we’re still early in the testing. But for the ADF looks very good and the excitement is quite significant. So in that trend, we’ll keep you update on what happens over the next quarters and how the initial safety testing turns out to be.

So as we stated in the past, we need to do first on safety testing and if only those are come out positive than we can continue with the other programs and clinical study. So let’s wait for the data and I think a lot of things can happen with them, if they stay excited as they’re at the moment..

Okay. And then just two quick ones on 24.

Can you remind me what you’d expect from a single dose of cetuximab trial safety signals goes, modular equivalent EGF inhibitory dose? And then in just in terms of – for the finalization of the go-forward molecule, I seem to recall at the last earnings call you presented this gold box structure – what progress you make on determining what the architecture go-forward architecture is for 24 and look forward for further update.

Thank you..

Yes. I’m answering the last one. So we are progressing with new molecules indeed so you’re correct. And as soon as we have the IP secured, we can publicized all that and give you more insight into what we’re doing there. But the structures are up and running, so we haven’t identified our lead candidate, so the program is progressing well.

But we have basically when we have investigated all that from a patent point view, we realize that we have an opportunity to gain possibly a very broad patent protection, much just beyond a molecule protection and our platform protection and that’s why we can’t get the augmented. So it’s purify peer reason and for no other reason.

But the molecules are progressing well. In terms of cetuximab tox data, we’ll have to go back and see if they have published single-dose tox data. I don’t know and if we know there are multiple dosing tox data in that context and we know that toxic doses – basically they saw toxicity in monkey after multiple dosing after already a few weeks..

Yes. I don’t know what that’s the question. I need to – can you repeat for cetuximab question. I’m not sure it’s kind of….

So you two have a very clean safety signal from a single dose AFM24, but I’m wondering what the comparable data with cetuximab obviously, it’s a completely different half-life. But what is the safety signal from a single-dose cetuximab at a roughly more or equivalent to the EGF inhibition..

Okay. So even with a single-dose – I can tell that from a clinical perspective there is a lot even with a single-dose of Erbitux triggers skin toxicity.

So in essence the fact that we didn’t see any differentiates the product already from Erbitux, it doesn’t – there is no necessary that – I mean it doesn’t need repetitive dosing to induce a skin toxicity by cetuximab. So we see there a different already.

And we have doses and we have testes a significant amount of AFM24 as we – in the same range doses that were adjusted for every capsule. I would think that it already gives us some confidence, that we did have a different safety profile there..

And Nick, we’re presenting a poster in a couple of weeks some now at a conference with more details on that study. And that will be not just single-dose there but also repeated dose. So in that context, that is more work coming along on AFM24 and as I mentioned before I think the conference end of June in Florence where we’ll talk about that..

And so that’s – multi-dosing denote?.

Correct..

Okay. Excellent, thank you very much..

We shall take our next question Hartaj Singh from Oppenheimer. Your line is open. Please go ahead..

Hi, this is Emma on for Hartaj. Thanks for taking the questions. So on AFM24 on the fourth quarter call, you indicated that you would be outlining the development strategy some time during the first half of this year. So now that we’ve seen this favorable tox data at AACR. I guess when can we expect further clarity on that clinical development task.

And specifically could you just walk us through any potential gaining factors in IND filing and what that potential timing might look like..

Yes. We’ve plan to give you an update in the next earnings call on the detail..

Okay. Thank you..

Thank you. I think there are no further calls..

Ladies and gentlemen, as there are no further questions at the queue. I would now like to turn the call back to Adi Hoess for any additional or closing remarks..

Yes, I want to thank all attenders and listeners to our call. And wish you a nice day. Bye-bye..

That will conclude today’s conference call. Thank you for your participation. Ladies and gentlemen, you may now disconnect..