Adi Hoess - Chief Executive Officer Florian Fischer - Chief Financial Officer Leila Alland - Chief Medical Officer Anca Alexandru - Head of Communications.

Do Kim - BMO Capital Markets Maury Raycroft - Jefferies Yale Jen - Laidlaw & Company Jim Birchenough - Wells Fargo Peter Lawson - SunTrust Robinson Humphrey Unknown Analyst - Unknown Firm.

Good day and welcome to the Affimed First Quarter 2018 Financial Results and Corporate Update conference call. Today’s conference is being recorded. At this time, I would like to turn the conference over to Anca Alexandru. Please go ahead..

Thank you. I’d like to welcome you to our investor and analyst call on the results for the first quarter of 2018. On the call with me today are Adi Hoess, CEO of Affimed who will present a corporate update, and Florian Fischer, Affimed’s CFO who will walk you through the financials.

Also on the call is Leila Alland, Affimed’s CMO who will be available for questions in the Q&A session. Before we start, please note that this call and the Q&A session contain 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 titled, Cautionary Statement 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 a corporate update..

Thanks a lot, Anca. Affimed has multiple ongoing clinical stage programs built on our antibody platform that are advancing in Phase I and Phase IIa studies.

The NK cell engager, AFM13 is being developed to treat CD30-positive malignancies and has shown a favorable safety profile as monotherapy and in combination with pembrolizumab, as well as emerging efficacy data.

The T cell engager, AFM11 is being developed to treat CD19-positive B cell malignancies and we are evaluating safety and preliminary efficacy in two Phase I studies in NHL and ALL.

Furthermore, a second T cell engager based on our platform is being developed by Amphivena to treat CD33-positive malignancies such as AML in a Phase I dose escalation study through recently introduced Redirected Optimized Cell Killing platform - ROCK in short.

This is a highly customizable NK and T cell engager platform and two pre-clinical stage programs have led to candidate entering IND enabling studies.

Furthermore, to accelerate our pipeline development, we have formed partnerships with industry academia and advocacy groups such as Merck, the MD Anderson Cancer Center, Columbia University, the Leukemia and Lymphoma Society, just to mention a few of our collaborators. Slide 4 shows our unencumbered clinical and pre-clinical pipeline.

All of our NK cell engagers bind to CD16A on NK cells while for T cell targeting, the engagers bind to CD3 on T cells.

Our lead product candidate, AFM13 has shown positive efficacy data as monotherapy in Hodgkin’s lymphoma and also in CD30-positive lymphoma, which we believe represents a novel opportunity with limited competition, for example in anaplastic large cell lymphoma or peripheral T cell lymphoma.

We have also reported encouraging efficacy of AFM13 in combination with the checkpoint inhibitor, Keytruda. I will provide more detail on the clinical data for AFM13 in this call. Our EGFR targeting NK cell engager, AFM24 has the potential to widen the therapeutic window and address the patient population resistant to standard of care.

We are developing AFM24 as a first-in-class NK cell engager in solid tumors and believe that AFM24 also has the opportunity to improve efficacy of checkpoint inhibitors. AFM26 is a BCMA specific NK cell engager that we are developing in multiple myeloma.

In particular, we aim to leverage BCMA as a target in autologous stem cell transplant-eligible patients, a setting where we believe NK cell engagers represent a well-differentiated opportunity.

Our T cell engager, AFM11 confers a well-differentiated approach for CD19-positive malignancies, in particular for the treatment of diffused large B cell lymphoma and mantle cell lymphoma. We believe that AFM11 represents a great opportunity for Affimed with the potential to pave the path for fast market approval.

A second T cell engager program based on our platform called AMV564 is being clinically developed by Amphivena, a company of which we own about 18.5% fully diluted. Slide 6, to the updates, as announced in March, Dr. Leila Alland joined us as Chief Medical Officer.

Her broad expertise in immuno-oncology and oncology will be instrumental to advance our product candidates through the clinic and for developing our future clinical development strategy. We’re happy to have Leila with us on the call today, and she will be available to answer your questions during the Q&A session.

Our longstanding supervisory board member, Rick Stead, has decided to step down from Affimed’s supervisory board effective June 19, 2018. We are very grateful to Rick for his valuable contributions during his 11-year tenure. Our supervisory board intends to nominate Dr.

Mathieu Simon, a seasoned immuno-oncology expert as a new supervisory board member, succeeding Rick. As you know from our fourth quarter 2017 update, in February 2018 we completed an underwritten public offering on the NASDAQ Global Market, raising a total of approximately €24.5 million in net proceeds.

In terms of platform updates, we’re very excited to have officially launched our ROCK platform. ROCK stands for Redirected Optimized Cell Killing. We officially introduced ROCK to the scientific community in two well-received presentations at the PEGS Protein Engineering Summit in Boston in early May 2018. I will talk more about ROCK later.

Throughout the first quarter, we have continued to progress our NK cell engagers through clinical and pre-clinical development as shown on Slide 7. In February 2018, we reported very encouraging data from studies of our lead candidate, AFM13.

We intend to present our next set of data from the AFM13 combination study with Keytruda at the 23rd Annual Congress of European Hematology Association - EHA in Stockholm in mid-June 2018. At the AACR 2018 Annual Meeting in Chicago, we presented data highlighting our progress toward novel EGFR targeting therapies.

We showed data on two development candidates from our AFM24 program, which are based on our ROCK platform. We anticipate completing IND enabling studies for one of the candidates by mid-year 2019. We continue to advance our AFM26 lead candidate through pre-clinical development.

This BCMA targeting NK cell engager is designed to address the medical need of eliminating minimal residual disease in patients with multiple myeloma. Again, leveraging our ROCK platform, we are developing several different antibody formats for AFM26.

Slide 8, regarding our T cell engager programs, we see a great opportunity with our differentiated proprietary formats which are highly specific, have unique PK/PD profiles, and do not confer non-specific activation of T cells in the absence of target cells.

While to date, several competitive programs presented with low objective response rates are being stopped, our two Phase I escalation trials of AFM11 are progressing well. Both our trials in patients suffering from NHL and from ALL respectively are actively recruiting patients as dose escalation continues.

Further clinical validation could come from Amphivena’s AMV564, a CD33/CD3 specific T cell engager based on our technology platform. Here, the Phase I study is ongoing and recruiting in AML.

Amphivena is also planning to initiate a study in myelodysplastic syndrome and is exploring the potential to address myeloid-derived suppressor cells in solid tumors.

Slide 9 ,we believe that the ability to utilize different antibody formats to activate innate and adaptive immune cells is a prerequisite to developing effective therapies for different cancers and other life-threatening diseases.

Our versatile ROCK platform meets this need and enables us to develop differentiated therapies aimed at improving efficacy and safety. We are very proud of our fantastic team who have employed their extensive drug development expertise to create ROCK. Its unique modularity is built on a proprietary toolbox and longstanding engineering know-how.

Specifically, the ROCK platform allows the generation of antibodies that target different tumor-associated antigens, use the ability [indiscernible], process long cell retention times, recruit NK cells through our anti-CD16A specific and T cells through our anti-CD3 specific epitopes, offer different PK profiles and show excellent stability and manufacturing features.

Importantly, the ROCK platform can suitably be applied for development of NK and T cell recruiting antibodies. Slide 10 shows in detail how our ROCK platform is built up and designed to reduce the complexity of antibody engineering.

ROCK employees a tool belt of scaffolds, linkers and antibody binding domains, and from these building blocks we can create very distinct antibody formats either solely comprising antibody variable domains or full length IGG scaffolds. The anti-tumor antigen binding domain can then simply be plucked into the antibody format.

Based on ROCK’s model in nature and versatility, we can engineer and assess different formats in parallel. Slide 11, our approach to high affinity CD16A targeting on NK cells is unique in the industry and allows us to address the needs of targeting malignant cells that escape elimination by current therapeutics.

We know NK cells are crucial in the body’s defense against pathogens and malignantly transformed cells.

While in the past most immuno-oncology approaches have focused on T cells as effector cells, in NK cell based approaches are becoming more and more widely investigated with a variety of different technologies emerging from both academic institutions and within the industry.

We believe that the overall progress in the field is very encouraging and recent data applications show signs of efficacy of adaptive transfer, or CAR NK treatment as presented, for example, at the recent Innate Killer Summit. To our knowledge, CD16A is the only receptor triggering ADDC and does not require an additional co-stimulatory signal.

Importantly, CD16A is constitutively expressed on about 95% of NK cells. Our approach is unique as our antibodies target a specific epitope on CD16A. We have optimized such CD16A binding to maximize NK cell mediated killing with more than a thousand-fold greater affinity to CD16A as compared to monoclone antibodies.

In addition, binding to CD16A is largely unaffected by plasma IgG, a major hurdle for NK cell activation by IgG-based therapeutic antibodies. This is particularly important as in the ground state, CD16 on innate immune cells is occupied by polyclonal plasma IgG.

This creates a significant threshold for IgG-based therapeutic antibodies as there is a huge excess of plasma IgG versus therapeutic antibody, however not for Affimed’s CD16A targeting antibodies.

The unique epitope recognized by our NK cell engagers results in them being virtually unaffected by plasma IgG; furthermore, CD16A binding is independent of valine phenylalanine polymorphisms, and finally our highly specific NK cell engagers do not bind to CD16b on neutrophils, avoiding a sync effect.

We believe that these features are highly important in targeting malignant cells which escape elimination by current therapies, for example cells with low target expression. Slide 12, a virtual lack of affection by IgG competition on cytotoxicity is shown here on the right side.

While Affimed CD16A ROCK molecules are virtually not affected, IgG-based monoclone antibodies show a very potent competition of cytotoxicity by polyclonal IgG, thereby preventing NK cell killing. Our approach is introducing a potent novel mechanism of action that we are using for a variety of antigens, as I’ll describe later.

On the left side, you can see that our proprietary NK cell engagers are designed for efficient cell killing even at low target BCMA expression of a few hundred receptors per cell. All of these features result in overall increased potency and efficacy. Slide 13, we believe that optimal I/O approaches build on both innate and adaptive immunity.

Tumor immune evasion impairs both NK and T cell function and therefore optimal I/O approaches should build on both immune systems. NK and T cells are very different in how they recognize a tumor.

While an NK cells shows non-specific recognition, T cells are only active once they can specifically recognize a tumor, hence the mechanisms by which a tumor can prevent destruction are very different.

While for NK cells, the inability to recognize tumor cells may be the key mechanism, for T cell it is the inhibition of the activation, for example through checkpoint inhibitors. In this context, we have generated data in Hodgkin’s lymphoma, both in vivo and in patients combining treatments targets innate and adaptive immunity.

As mentioned earlier, we are generating clinical proof of concept for our NK cell engager approach by developing our lead candidate, AFM13 as mono and combination therapy. In the past, we have reported data showing that we have observed clinical efficacy in both the mono and combination therapy setting.

AFM13 has already demonstrated evidence of safety and clinical efficacy in heavily pre-treated Hodgkin’s lymphoma patients in a Phase I study, and three clinical studies for AFM13 are currently ongoing.

In a Phase IIa in relapsed refractory Hodgkin’s lymphoma led by the German Hodgkin’s Study Group, the favorable safety profile was confirmed and single agent activity was demonstrated in patients failing standard treatment, including [indiscernible].

In February, we reported data from a Phase Ib/2a IST in relapsed refractory CD30-positive lymphoma led by Columbia University. Here, single agent activity was demonstrated, including one complete response, one partial response, and one stable disease in the first cohort, comprising three patients.

These results are very encouraging as they provide further evidence that NK cell engagers are monotherapy are able to induce tumor regression in this indication. In general, we view CD30-positive lymphoma as an attractive indication that may broaden the potential of AFM13. Both ISTs are open and active recruiting patients currently.

We’re also conducting a Phase Ib study of AFM13 in combination with Merck’s Keytruda in relapsed refractory Hodgkin’s lymphoma. As previously reported, the combination was well tolerated with most of the adverse events observed mild to moderate in nature and manageable with standard of care.

To date, we reported best response preliminary data for nine patients showing objective response rate NCRs which compare favorably to historical data of anti-PD1 monotherapy alone in a similar patient population. We observed an ORR of 89% and a CR rate of 44%.

In this study, recruitment has been completed and we intend to present the next data set at EHA in mid-June. Slide 15, we believe that our AFM24 program promises to be a well differentiated I/O therapy to current standard of care treatment, such as cetuximab.

Through our molecules’ binding modality and the resulting immune effector cell activation, our molecules are differentiated from cetuximab by their immuno therapeutic mechanism of action.

In these molecules, the EGFR binding domain was selected to minimize inhibition of EGF receptor mediated signal transduction with the aim of achieving therapeutic efficacy while lowering the risk of side effects, such as skin toxicity, that are associated with anti-EGFR monoclone antibodies.

The approach of NK cell mediated targeting of EGFR expressing human cancers introduces a novel, highly potent effector function to address the needs of patients who may not benefit from anti-EGFR monoclone antibodies.

At AACR, we presented in vitro and in vivo data for two ROCK-based AFM24 candidates showing the first evidence supporting this new mechanism of action. We anticipate completing IND enabling studies for one of the candidates by midyear 2019. Slide 16 shows data from the two candidates. They are called AFM24I and AFM24T.

Both candidates bind with high affinity to primary human NK cells in the presence and absence of polyclonal IgG, which is shown on the top right. On the bottom right, AFM24I demonstrates potent tumor growth inhibition at different concentrations.

Slide 17 summarizes our work for AFM26, which we are developing as an NK cell engaging bispecific antibody targeting B cell maturation antigen. We are addressing the medical need in multiple myeloma. Pre-clinical development for our candidate based on the ROCK platform is ongoing.

Slide 18, as mentioned earlier, our tetravalent multi-specific antibody platform has several differentiating features and offers the potential to overcome the challenge to find the optimal therapeutic window with a T cell engager.

Differentiating features include no non-specific activation of T cells in absence of target cells, targeting tumor cells with very low target expression, lysis of tumor cells independent of number of T cells as well as significantly improved PK versus the BiTE.

Our lead candidate, AFM11 is in clinical development and we are in the process of determining the recommended Phase II dose. Two Phase I dose escalation trials are ongoing and actively recruiting patients with relapsed refractory ALL and NHL respectively.

With our T cell engagers, we have the potential to pave the path to fast market approval in indications such as diffuse large B cell lymphoma and mantle cell lymphoma. As mentioned earlier, we have a second program that’s developed by Amphivena called AMV564 which is a CD33/CD3 specific antibody, which is based on our technology platform.

Amphivena continues to recruit patients into its first-in-human Phase I dose escalation study with relapsed refractory AML. I will now hand the call over to our CFO, Florian Fischer, who will provide further details on the financial figures..

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 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 euros. Any numbers referring to Q1 2017 and Q1 2018 are unaudited.

Cash and cash equivalents totaled €55.3 million as of March 31, 2018 compared to €39.8 million as of December 31, 2017. The increase was primarily attributable to the net proceeds of €19.7 million from public offerings partially offset by Affimed’s operational expenses.

Net cash used in operating activities was €6.9 million for the first quarter 2018 compared to €7.2 million for the first quarter of 2017. Cash flow from financing activities amounted to €22.6 million for the first quarter of 2018 compared to €16.4 million for the first quarter of 2017.

Affimed expects to have cash to fund its operations at least until the fourth quarter of 2019. This provides runway for the planned development of our clinical programs as well as for further discovery and early development activity. Revenue for the first quarter of 2018 was €500,000 compared to €400,000 for the first quarter of 2017.

Revenue in both periods was derived from Affimed’s collaboration with LLS and the AbCheck service revenue. R&D expenses for the first quarter of 2018 were €6.4 million compared to €5.4 million for the first quarter of 2017. The increase was primarily related to higher expenses for AFM11 pre-clinical programs and infrastructure.

G&A expenses for the first quarter of 2018 were slightly lower with €2 million compared to €2.2 million for the first quarter of 2017. Loss for the first quarter of 2018 was €8.2 million or €0.15 per common share compared to a loss of €7.8 million or €0.19 per common share for the first quarter of 2017.

The increase in loss was primarily related to higher spending on R&D for AFM11 pre-clinical programs and infrastructure. I will now turn the call back over to Adi for a summary of our two clinical programs and our pipeline.

Adi?.

Thanks a lot, Florian. Our strategy is to maximize the value in our unencumbered clinical and pre-clinical pipeline of NK and T cell engagers as well as from our platform.

We are expanding our leadership in NK cell mediate tumor cell killing by leveraging our lead product, AFM13 as monotherapy in CD30-positive lymphoma and in combination with Keytruda. Based on the encouraging clinical data, we are currently planning follow-on clinical studies.

The clinical data for AFM13 are further stimulating the generation of an NK cell engager pipeline and we are advancing further pre-clinical candidates such as AFM24 and AFM26.

Another focus of our activities is the exploration of NK cell engagers in combination with adaptive NK cells or immune activating agents such as IL-2 and IL-15, as we have previously mentioned.

We are also advancing T cell engagers and our lead molecule, AFM11 is being investigated in the studies that I mentioned before with a goal to identify the MTD and achieve proof of concept. Indeed, we are also planning follow-on clinical studies for AFM11. With Amphivena’s AMV564, additional POC is possible in AML.

Having developed our ROCK platform, we can now continue to broaden our engager pipeline and will leverage our pipeline and technologies to create value through next generation products and partnership opportunities. On Slide 21, you can see an overview of our executive team, which we have strengthened considerably over the last year.

We are a joint European and U.S. team, combining big pharma and biotech expertise as well as program planning and execution of immuno-oncology clinical development and, importantly, also commercial strategy and business development expertise. Thank you very much for your interest, and the call is now open for questions..

[Operator instructions] Our first question today comes from Do Kim of BMO Capital Markets. Please go ahead..

Hi, thanks for taking my questions.

On the AFM13 update that you’re expecting at EHA, could you tell us what we should expect in terms of data? Will you have results for all 24 patients?.

Leila, are you going to jump in here, please?.

Yes, I’ll jump in. So as Adi said, we will be providing an update at the EHA meeting in mid-June, and we will have data on approximately 18 patients at that meeting. This will include data which includes at least three months data from all 18 patients, so it’ll be the most up-to-date data that we have.

We’re currently compiling that data and we’ll be ready to present that in mid-June..

Great, thank you. I wanted to ask about the ROCK platform.

Are your plans to use that exclusively for internal drug development, or is there a strategy to potentially find partners for drug discovery to license externally?.

Thanks for this question, it’s a very good question. Indeed, one of our strategies has been with learning of how our molecules work in the clinic, is then to specifically design molecules that may have different features, so that work has been ongoing since a while and resulted now in the ROCK platform.

We primarily obviously did that for our own benefit, because the AFM24 and AFM26 are based on that platform and we have carefully designed these molecules to address specific settings, so that was the first intention that the result of the platform was always aimed to be a platform used for product development, indeed for Affimed targets.

Obviously, there are more opportunities out and we are now sharing the data with the broader industry. That’s why we gave two presentations at the PEGS meeting and we are currently collecting feedback on that.

But again, we may do certain collaborations with third parties, but we are not a service company that now broadly gives access to multiple targets, so we will do this in a very detailed manner where a party may have an interest to do a significant collaboration with Affimed. That’s our strategy currently that we will pursue..

Great, thanks Adi. Looking forward to your future updates..

Thank you, Do..

We will now take a question from Maury Raycroft of Jefferies. Please go ahead..

Hi, good morning, and congrats on the updates. Excited to see the additional data at EHA. I guess maybe just a few points of clarification around the EHA data for the AFM13 combo.

For some of the patients, will we see six-month follow-up?.

Again, Leila?.

Yes, sure. As with any clinical study, patients have been enrolled for a range of time, depending on when treatment began, so what we’ll be presenting at EHA is patients who have been on study for a minimum of three months and some of whom will have been on study for longer..

Okay, great.

As far as the six additional patients who I believe have been enrolled, so if those patients have been treated, would you potentially top line all 24 patients around the EHA update, so maybe you have the 18 in the EHA presentation but then have all 24 included in some sort of press release outside of the conference? Is that possible?.

No. We have guided to anticipating full three months data by midyear and full six months data toward the end of the year. We’ll be presenting the most up-to-date data at EHA, which will include the data on approximately 18 patients..

Got it, okay.

Then for next steps with meeting with the regulators, what will be the expectations going into that meeting, and what will you be trying to accomplish with that?.

Is your question in relation to AFM13?.

Yes, for the combo. I think that was--at some point, there was some guidance around that, that there would potentially be a meeting with regulators following the AFM13 combo data, so I’m just wondering if there’s any additional clarity on if that would happen, and if there’s some sort of expectations for what the meeting would be..

Okay, thank you. We are in the process of establishing our clinical development strategy moving forward, and this includes interactions with regulatory authorities as well as with all of our stakeholders, including our investigators and our KOLs, and of course our collaboration partner, Merck, our collaborator for the combination study.

We will update you in due course when these plans have been solidified..

Okay, sounds good.

As far as--I don’t know if you can comment on this or not, but for the EHA data for the combo study, is that going to be an oral presentation or a poster? Can you disclose that?.

We’ve been notified that it has been accepted for poster presentation..

Got it. Last question is based on the T cell lymphoma trial.

Is it possible that we could see data from that at EHA as well?.

As you know, this is an investigator-sponsored study, and we’ve been working closely with the sponsor of the study to provide regular updates of the data. We will not have additional data to be presented at EHA..

Okay, sounds good. Thank you very much for taking the questions, and I’ll hop back in the queue..

Thanks a lot..

We will now take a question from Yale Jen of Laidlaw & Company. Please go ahead..

Good morning and thanks for taking the questions.

Just in terms of the ROCK platforms you recently developed, could you give us some sense, maybe quantitatively, to compare with the earlier version or the original version of the NK engager, so we may see some quantitative differences or any specific attributes that was the improvement? In other words, a little more color on this platform..

Yes, thanks Yale for this question. Indeed, we are--how does the platform work now, so what--.

As I have indicated, there is a toolbox of scaffold linkers antibody domains, and what we have been doing over the past years is we have generated a very significant amount of very different molecules, some are IgG based, some are just based off Fc binding domains, as our interests is of antibody binding domains.

What our goal was that we can identify a minimum number of scaffolds that are very different, and I guess they are shown in the presentation how they differentiate, so some have full length ITTs, other incorporate the [indiscernible] motive, others just have a tetravalence structure.

What we are doing is that we can use a very small number of these validated formats, plug in antibody binding domains, and then have a set of, let’s say, five, 10, 15 very different molecules and not just a [indiscernible] as we have previously available.

Then we’ll take these molecules forward, of which we already know that they are stable, that they are well manufactured, and then we profile them in a variety of assays, so in the beginning you would not have to make a choice either to go for whatever I call it - Form A, B, C or D, you will just take, as I say, this small number of antibodies that all are EG directed against the tumor antigen, compare them in a variety of assays, and then at the end you can decide which one you’re going to take forward.

How are they differentiating? They are differentiating by affinities, they are differentiating by their bidistribution, they are differentiating by their PKs, so they all have features that can influence uptake into the tumor, that can also influence dosing regimes.

This is the versatility that we have available, and we can take a conscious decision on which is the best candidate after we have generated data. I hope this helps on how we are employing it, and that we do not have to pick a particular antibody format in the first place..

So it potentially gives you a broader variety sort of end prospects to be chose from or screened from, as well as it is a platform that maybe technically it’s easier to assemble a large number of a variety of things, instead of the more specific process that has been used [indiscernible] process being used before.

Is that a fair way to think about that?.

Yes, exactly. This puts a much broader footing in terms of how these molecules now are comprised of, so as I said, they all have different features.

We’re exploring them in parallel, and as I said, the [indiscernible] are part of ROCK as much as IgG structures are, or what we call [indiscernible], so there’s an enormous versatility in this platform and the eventual candidate is then picked based on a target product profile.

But many of--as I say, all of these candidates would already qualify in principle to be within the target product profile, but only the final molecules that we have available then can be tested..

Maybe just one follow-up here, I believe you mentioned that 24 is selected or processed from the ROCK process, and is 26 also the same way? The follow-up question beyond that is going forward, are you going to revamp some of these, for instance existing 11/13 to a more--a greater versatility type of screening process for going forward?.

It’s a very good question. Indeed the first half of your question is 24 and 26, yes, they are indeed based on the ROCK platform, but each of the respective programs always comprise an antibody that’s based on a IgG domain but it’s also just solely based on antibody binding domain.

So we have still the full breadth of different kind of antibody modalities available, both for AFM24 and for AFM26. Another good question is how would we go back to AFM13 and AFM11? Let me give you an answer specifically for AFM11.

What we have learned in the field is that we have currently seen efficacy of T cell engagers based on a BiTE, so this is Blincyto, and there is some sort of proof of concept also available from a DART.

These are based--these are both fairly short lived molecules that are given by continuous infusion because their half life is in the range of just a few hours.

There have been platforms developed that have longer half lives, so they are based on IgG formats, but as the companies have reported, either ORRs were not high enough or some of the programs even have to be stopped.

So for T cell engagers such as AFM11 or even AMV564, the structure we have available currently may already be a quite good one, and that’s why we are progressing AFM11 and we are not thinking in that direction, that we need to have a replacement for AFM11 based on another ROCK molecule.

So T cell engagers, NK cell engagers, as I say, they go through a very thorough process, then we check the TPP and the candidates we have available, and those that are generated do in our mind fulfill the TPPs so that we eventually can bring these products, if they are potent enough and safe enough, to the market..

Okay, great. That’s very helpful, and thanks for answering my questions..

We will now take a question from Jim Birchenough of Wells Fargo. Please go ahead..

Hi guys, thanks for the detailed update, and congrats on all the progress.

A question on AFM11, can you remind us where we’re at in the dose escalation and if we’re at a dose that one would expect efficacy, and then ultimately when you think about the dose range that’s being explored here, at what point do you think we’ll be able to benchmark against Blincyto or even against the CD19 CAR Ts? Thanks..

Leila, do you want to jump in here, or shall I?.

Sure, I’d be happy to. Thank you for the question. Both studies are actively recruiting patients and dose escalation continues for both studies. We are currently in dose level 4 for the NHL study and in dose level 5 for the ALL study.

We plan to complete dose escalation and once we have completed this, we will be able to provide a more meaningful update, including the comparison of our data compared to what would be expected with Blincyto.

I believe we’ve mentioned in the past that based on pre-clinical data, we could reach potentially active doses somewhere between dose level 5 to 7, but of course it’s difficult to predict from pre-clinical--such clinical data.

We have not guided to a specific time point at which we will be presenting data, but dose escalation continues, as I said, for both studies and we’ll have a lot more data available as the year progresses..

Leila, just on AFM13, we’ve got the three-month update for 24 patients by midyear and six-month by year-end.

Do you need that six-month update to advance discussions on a Phase II, or is the three-month data sufficient to have those discussions with FDA and initiate a Phase II?.

We’re actively having those discussions currently internally and with our stakeholders. I think we have ongoing discussions with regulators, so I don’t think we’re looking for a specific dataset coming to trigger those activities, no..

Then maybe Adi, just on the ROCK platform, can you say whether that platform might accelerate the process from discovery to IND filing? What’s that current timeline, and could ROCK with this modular platform accelerate that, do you think?.

Yes, thanks a lot. That’s a very good question, and indeed it does, so this modularity and versatility allows us to generate lead candidates indeed very quickly, so if we have an antibody binding domain available, we can just pluck that in, then profile these candidates next to each other and then initiate research [indiscernible] generation.

I mean, there is always an optimal scenario, and when I mention timelines, always my researchers are jumping on my throat, but it’s indeed a very straightforward process so you can imagine engineering new antibodies by plugging in antibody binding domains, you can do it in a few months and then when these candidates are really stable and effective, then you can just go ahead with initiating IND enabling studies.

So exact timelines is always hard to predict because this also relates to the specific target, the other assays available that are required, but it’s at least as fast as generating monoclone antibodies. .

I was going to ask about timelines, and I will - I understand you might not be able to answer.

For AFM24 and AFM26, do you have a target time frame for IND enabling studies for each of those?.

Yes, we do. We have announced it for indeed AFM24, so there we are planning to have the IND by midyear 2019. For 26, we haven’t yet announced, but for AFM24 we did..

Got it, great. Thanks, and appreciate all the detail. .

We will now take a question from Peter Lawson with SunTrust Robinson Humphrey..

Hi Adi.

Just on AFM11, do you think we could get data from NHL patients first or ALL, and any color around the line of patients you’re seeing in the dose escalation for both of these?.

Leila?.

Yes, so I’m pleased to say that we have two studies that are dose escalating in parallel, one with NHL patients and the other with ALL patients, so it’s a little bit difficult to predict which one will show activity first, but fortunately we have not taken a sequential approach but we’ve taken a parallel approach and so we’re gathering data for both patient populations..

So again--sorry Peter, just something here. You may recall that in the past, studies were not progressing as fast. There were different reasons associated with that.

We have addressed all these in the meantime and the progress is indeed very good, so what we’re asking is a little bit more patience before we are--as I say, before we are coming to more solid data in the dose escalations as they are ongoing, and then we can inform you. So we’ll keep you updated on that as we progress..

But we shouldn’t think about those--it’s more of a 2019 event, do you think?.

In terms of timing, again we’re not at the moment committing to any timelines in essence.

As Leila has said, we are approaching active dose levels from our pre-clinical experiments, dose levels 5, 6, 7, You can see that, as Leila just said, we are approaching or we are in the midst of these dose levels, so it is a T cell engager, in essence meaning that these are molecules that are very potent and things are progressing well on our end, so in terms of being more precise, it’s very challenging to be so, but on the other side it’s progressing well so we’re accumulating data on our end..

Got you, thank you.

Then I guess in AFM13 for Hodgkin’s lymphoma, how do you see the kind of commercialization path in disease that’s relatively well controlled, it’s got a lot of, I guess, ATC, kind of I/O options? Where you see AFM13 fitting into that paradigm?.

There are still a significant number of patients that are not cured, especially patients that relapse refractory to stem cell transplants, so any third, fourth, fifth line patient, even if other therapies are available, these patients indeed go on these therapies but eventually they relapse, so the market opportunity remains.

Here, it’s rather dependent on how your efficacy is perceived and how the durability of response is perceived, and that’s what we are currently generating. We are not concerned about the market opportunity at that stage.

We are seeing good data on AFM13 relating to safety and efficacy - when I mean good, it’s very encouraging, what we have reported, and so basically that gives us a lot of energy in order to bring these molecules forward.

So overall, both in the setting of T cell lymphoma and Hodgkin’s lymphoma, there is a very reasonable market opportunity in the relapse refractory setting..

Then I apologize if I missed this, but the CD30-positive lymphoma, any color around the enrolment there? We’ve had some nice initial data, very nice initial data in February.

When could we get the next update, and any color around CD30 and how that’s panning out?.

Yes, we have said in the past [indiscernible] we are only recruiting patients that have cutaneous lesions, so there is a very specific subset of patients that we allow to enter this study, for the reason that we are taking serial biopsies.

We had originally mentioned that we were working with the investigator to present these data, and our original plan was to have something available in the second half of 2018..

Got you.

Is there a particular venue or it’s going to be a top line thing?.

As I said, that’s too premature how we want to do that, but the one thing we can tell you is that there is significant excitement by the investigators on the conduct of the trial, so we’ll just choose it as soon as all data are available..

Got you.

Is there any way you can disclose how many patients you’re going to be looking at there?.

Originally we had said that we are treating a minimum of nine patients, but there’s always an option that we can expand that. As you may recall in the beginning of the year, we have raised cash that would give us the opportunity to expand especially the CD30-positive lymphoma indication, so those are the things that are currently ongoing.

Just to give us--if we can’t be precise enough because these are all ongoing discussions, we’re just, as Leila has mentioned, bringing all these things together and then we can lay out these plans in much more detail. But as I have said on one of my last slides, we are planning ahead now for both AFM13 and AFM11 the next set of clinical studies. .

Got you. Okay, thanks so much. Thanks for taking the questions..

Thanks Peter..

We will now take a question from [indiscernible] of [indiscernible]..

Yes, hello. Thank you very much for taking the question. I have one short question about the ROCK platform.

Do you any suggestions what is with the MHC peptide molecule that is not on your pipeline anymore?.

Yes, we have a variety of earlier stage programs. Amongst that is the MHC targeting peptide, so we have worked on that in order to show that it can make antibodies against very challenging targets.

We have then converted these antibodies to both NK cell and T cell engagers and could again demonstrate that we have the opportunity to eliminate cells with low target expression, but obviously our resources have to be focused. We see in the meantime much more activities for AFM13.

We have just described the encouraging opportunities with our combo study, also with the T cell lymphoma study, so that’s where we are focusing. AFM11 is progressing very nicely, so again that’s where our commitment has been given to, and on top of that we have moved along 24 and 26 now to substantial maturity on the pre-clinical side.

So we are focusing on those programs for the time being as lead candidates, but obviously there are earlier stage molecules that we’re not sharing with the public domain at that stage, but obviously we are discussing that with potential industry partners..

I suppose the new ROCK platform does not inhibit these molecules but would enable them as well?.

Yes, the ROCK platform is just broadening the opportunity of selecting very different molecules, so this is rather making it more likely to identify development candidates against specific targets.

But what we have been doing is we have identified certain indications, tumor indications that the need is to eliminate cells with very low target expression, so some reasons for the resistance is not that you have cells reoccurring that are target negative but it’s just very low.

We are seeing this with BCMA over and over again, that there are patients that present with cancer cells that just have 100 copies and we know that conventional technologies, IgG based, so regular monoclonal antibodies or antibody drug conjugates would not really be suitable to eliminate such cells.

This is where our focus has been and the ROCK platform has been optimized towards such applications. .

Okay, thank you very much. That helps a lot..

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

Yes, thanks to all of you for listening in on our Q1 financial earnings call. I appreciate all your questions, and as we’ve said, we are very happy to have made significant progress with our programs, both clinically and pre-clinically, and also have presented this new platform, and you could see the lively discussion that there is quite excitement.

Thanks a lot..

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