Anca Alexandru – Head-Communications Adi Hoess – Chief Executive Officer Florian Fischer – Chief Financial Officer.

Yale Jen – Laidlaw & Company Nick Abbot – Wells Fargo Do Kim – BMO Capital Markets Maury Raycroft – Jefferies Peter Lawson – Suntrust Robinson Humphrey.

Good day, welcome to the Affimed Third Quarter 2017 Earnings 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 and the results for the third quarter of 2017. On the call with me today are Adi Hoess, CEO of Affimed, who will present the corporate update and Florian Fischer, Affimed’s CFO, who will walk you through the financial.

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 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. And good morning all and thank you for listening to our third quarter earnings calls. As you know Affimed develop an immune cell engagers that eliminates tumor cells by engaging and activating Natural Killer-cells or T-cells.

Our clinical and pre-clinical pipeline is based with [indiscernible] molecules with tetravalent bispecific antibody format. 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 are particularly interested in unlocking the full potential of NK-cells immunoncology through suitable combination approaches. Here we are aiming on the one hand to generate a conservative immune response through combinations of synergistic mechansims for instance by combining our products with checkpoint inhibitors or cytokine.

On the other hand we can increase the number and activity of NK-cells available for an immune response via adoptive transfer. To this end, we have formed several collaborations with industry and academia.

We also have a well differentiated seasonal based approach which includes our own clinical candidate AFM11 and we will provide an all our clinical programs as well as our preclinical programs to date.

Slide 4, we can unincumbent clinical and preclinical pipeline of NK-cell 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 our own clinical development. The second T-cell engager program based on our platform called AMV564 is being developed by Amphivena Therapeutics, a company of which we own about 18.5% fully diluted. AMV564 has recently entered clinical development in AMLs.

Slide 5, in September 2017, we make a significant addition to our management team, Wolfgang Fischer, joined Affimed as Chief Operating Officer from the Novartis Group. There he most recently served as Global Head of Program and Project Management of Sandoz biopharmaceuticals division.

Wolfgang has over 20 years of R&D experience with a focus on oncology, immunology and pharmacology. With his proven track in drug development he will support us in advancing our programs to address the existing medical need in hematologic and solid tumor indications.

In addition to his role as COO, Wolfgang has been working closely with our clinical teams since joining in September and he will now formerly assume a responsibility as interim CMO.

Regarding our T-cell engager programs, we’re conducing two clinical Phase 1 dose estimation trials with AFM11, CD3/CD19 target in tetravalent bispecifi T-cell engagement in patients with replased and refactory ALL and with relapsed refractory non-Hodgkin lymphoma respectively.

Those studies are ongoing and recruiting into the four dose cohorts for ALL and into the third dose cohorts for NHL. Recruitment is also ongoing for a first in human Phase 1 dose escalation trial of AMV564 conducted by Amphivena, in patients with relapsed refractory acute myeloid leukemia.

AMV564, a CD33/CD3 specific antibody, based on Affimed’s technology platform. Preclinical is planned to be presented on AMV564 at the upcoming ASH Annual Meeting. Slide 6, we have made significant headway in validating our NK-cell engager approach this quarter in particular to encouraging data from studies of our lead candidate AFM13.

AFM13 CD30/CD16A targeting tetravalent, bispecific molecule which were developed in as both mono and combination therapy. In our Phase 1b combination study of AFM13 with Merck’s KEYTRUDA in Hodgkin Lymphoma we have completed the dose escalation and the dose expansion cohort is open and recruiting.

Beta analysis of three months response rates from the escalation phase is ongoing and to date analysis of 9 out of 12 patients has been completed. The highest dose cohorts in the three patients analyzed to date were reporting partially metabolic response to adverse tumor.

I will provide more detail on the results a bit later on this call and we plan to present detailed dose escalation data at ASH in December. Columbia University is leading the investigate response of translational Phase 1b/2a study of AFM13 in patients with relapsed refractory CD30 positive lymphoma with cutaneous manifestation.

The first cohort, we enrolled and recruitment in further cohorts is ongoing. The first patients who suffers from anaplastic large-cell lymphoma with cutaneous manifestations has been analyzed and he has experienced a complete response of all cutaneous lesions after the first treatment. The systemic evaluation is still ongoing.

Again, I’ll provide more detail on the results a bit later on this call. We’re also investigating AFM13 in an investigators on Phase 3 monotherapy study in Hodgkin Lymphoma, which is being led by the German Hodgkin Study Group. This study is open to recruit under the new design which includes patients pretreated with [indiscernible] and PD-1.

We are also collaboration with the University of Texas, MD Anderson to evaluate AFM13 in combination with MD Andersons NK-cell product, research activities are progressing. Finally, we continue to grow and optimize our technology and has developed new tetravalent bispecific antibody format in addition to the TandAb format.

These molecules compare existing bispecific properties aiming at tailoring PK profiles. Based on our platform we are advancing AFM24 and EGFR/CD16A specific NK-cell engager and AFM26 targeting BCMA through and the enabling study. Final candidates have been selected for both programs. Slide 7, our platform is differentiated from others.

For our development of tetravalent bispecific molecules and the bivalent finding to two receptors and two different cells enables higher affinity findings through increased avidity while maintaining high specificity. We believe with this is very important in order to obtain favorable safety profiles.

Furthermore, our versatile platform are now also development of molecules with multi specificity and tailored PK profiles.

Further distinguishing our approach on most immune cells engagement approach is to be focused on T-cells, our platform will lively generate both T and NK-cells engagers allowing us to explore both adaptive and in making new mechanisms.

Slide 8, we believe that, therapeutic use of NK-cell function is another promising approach to eliminate tumor cells. NK-cells are crucial in the body's defense against pathogens and malignantly transformed cells and the positive correlation between NK-cell infiltration and clinical outcome in patients has been observed.

Yet, specific NK-cell engagement remains to be fully exploited for therapeutic use. We believe that we have identified a very promising target to address this and CD16A is a key activating receptor capable of arming NK-cell and high affinity targeting of a specific epitope on CD16A enables killing five NK-cells.

General proof of concept of NK-cells mediated tumor killing has been generated over the last years. For example, in a Phase 1 study, in relaxrefractory AML published last year and investigators reported CR in four out of nine patients treated with active NK-cells.

Safety and the ability to reduce emission in leukemia patient has also been demonstrated previously. It was described that in NK-cells are critical to graft versus leukemia effect, but do not unless its graft versus host. This has been seen consistently across studies looking at over 100 patients.

Slide 9, the mode of action of our molecules depicted here show that high affinity finding of CD16A redirect NK cytotoxicity to a specific tumor target. Tetravalent bispecific performance allows efficient finding in both NK-cell and tumor cell, bringing them into proximity and therefore overcoming the tumor’s ability to evate the immune cells.

Release of perforins and granzymes can be subsequently trigger tumor cell lysis. Slide 10 shows the preclinical data demonstrating the superior potency and efficacy of our tetravalent bispecific format. As compared to Fc-enhanced IgG are native IgG molecules, our molecules possess a higher potency as shown on the left.

Furthermore, in an in vivo PDX model, our NK-cell invasion in contrast to control molecules are able to hold the tumor growth as shown on the right. Our lead candidate, AMF13, has shown a very good safety profile in toxicity studies in cyno monkey and this has been supported by our ongoing clinical studies.

Slide 11, our approach of high affinity CD16A targets in running NK-cells is unique in the industry. CD16A is the only receptor triggering ADCC and does not require additional co-stimulatory signals. Importantly, CD16A has constitutively expressed on about 95% of NK-cells.

We have optimized CD16A volume to maximize NK-cell mediated killing with an upto 1000 fold greater affinity to CD16A, as compared to monoclonal antibodies. In addition, binding to CD16A is launching unaffected by competed IgG, a major hurdle for NK-cell activation by IgG based structures.

This is particularly important as in the grown state, CD16A immune cells this occupied by a polyclinical plasma IgG. This creates a significant threshold of IgG based on therapeutic antibodies as there is a huge excess of plasma IgG versus therapeutic antibody. However, not for CD16A targeting antibody.

The unit epitope recognized filing NK-cells engagers results in them being virtually punished by plasma IgG. Furthermore, CD16A binding independent of the unveiling seven element polymer assistance and finally highly specific NK-cells engagers do not find strategic [indiscernible] avoiding the so called general effect.

We believe that these features are highly important in targeting malignant cells which is case elimination by current therapeutics for example cells which have a low target expression. Slide 12, shows that our NK-cells engagers can kill tumor cells with very low target expression.

AFM13 in vitro killing the cells with CD30 expression as low as a few hundred receptors and – even a few thousand receptors and even a few hundred receptors per second. All these unique features result in overall increased potency and efficacy of our engager agent.

Slide 13, as mentioned earlier, we are generating clinical proof of concept for our own engagement approach by developing our lead candidate AFM13 as mono and combination therapy and I would like to show you now that we have observed clinical activity in both the mono and combination therapeutic setting.

AFM13 has already demonstrated based in clinical activity and have an Hodgkin lymphoma patients in our Phase 1 study. With tumor shrinkage observed in 62% of patients, which was 8 out of 13 and PRs in 23% of patients, which was 3 affected. None of the patients experienced in a PR has been previously treated with [indiscernible].

As previously communicated, statement from our investigation sponsored Phase 2a trial for AFM 13 in relapsed and refractory Hodgkin lymphoma which is led by the German Hodgkin study group show for the first time that AFM13 is acting as a single agent in a heavily pretreated group of patients and in particularly the AFM13 is active post for [indiscernible] partial responses were observed in two out of seven evaluated patients in growth under the study’s original protocol who has been pretreated with PV does not, anti-PD1.

In our Phase 1b trial, in the relapsed refractory and Hodgkin in combination with Merck’s, KEYTRUDA we have completed dose escalation parts of the trial with three patients enrolled into dose levels one and two respectively and six patients enrolled into dose level three through a previously communicated reported prior to infusions related reaction which was classified as [indiscernible].

With those expansion ongoing and the recruiting at the highest dose explored during those escalation. Data analysis of three months response rate from the escalation phases ongoing and to-date analysis of 9 out of 12 patients have been completed. Of the three patients enrolled into cohort one, three didn’t on PR while one patient progressed.

Of the three patients enrolled into cohort two, one patient experienced with CR one patient at PR and one patient progressed. Out of the six patients in cohorts, in dose cohort three, three were analyzed to date all of which experienced partial metabolic responses at the first tumor.

We are trying to present further data and post at the at the upcoming ASH meeting in December in 2017. Slide 14, we announced last quarter that Columbia University had initiated a translational study to evaluate AFM13 in patients where it’s relapsed and refractory CD30 positive lymphoma with cutaneous manifestation.

We call that this trial is designed to allow for zero biopsies thereby enabling assessment of NK-cells are all achieved and tumor cell killing within the tumor environment. The first cohort has been fully enrolled and recruitment into further cohort is ongoing.

CD30 positive lymphoma with cutaneous manifestation comprises a number of different sub indications and here we present data on the first patient suffering from ALCL with cutaneous manifestation. These images show a skin lesion on the left shoulder of the patient which was already significantly reduced on day three post treatment start.

By day 21 post treatment start the patient had experienced a CR of all cutaneous lesions. The systemic evaluation has been ongoing, but these results are very encouraging as this provides first evidence that NK-cell engagers are able to infuse tumor regression in this indication.

In general, CD30 positive lymphoma as an attractive indication that may broaden the potential of AFM13. Slide 15. Additional opportunities for our NK-cell engagers and acute combinations with NK-cells transfer.

Expansion and stimulation of [indiscernible] NK-cells followed by reinfusion and combination with NK-cell engager and novel therapeutic concept. And this combination large preactivated NK-cells can be redirected by our NK-cell engagers to recognize malignant cells.

This approach is independent of patient on NK-cell count and has potential ability at the time of autologous stem cell transplant. We are investigating this approach with our partner MD Anderson. Initially we plan to investigate AFM13 with MDACC’s NK-cell program in the transplant setting.

Preclinical research activities are on track and these are intended to be followed by a Phase 1 clinical trial proof of concept for this combination with AFM13 in Hodgkin Lymphoma may pave the way for combination in further indications such as multiple myeloma.

We hold an option to exclude the [indiscernible] rights to develop commercialize any further development under the clinical. In addition to our clinical programs, we have an innovative preclinical pipeline addressing both hematologic indications in solid tumors.

Over the last quarter, we have further characterized our tumors advanced preclinical candidate AFM24 and AFM26. Slide 16, despite several marketing agents, such as cetuximab and kinase inhibitor there is a significant medical need for a novel approach to treat each positive tumors.

This requires widening the therapeutic window and addressing treatment resistant. Existing drug functions were blocking with signaling activity of each cell. Our approach is different because we are pursuing EGFR as a target to increase immune cell killing at the size opportunity.

Our goal is to address the limitations of existing drugs by improving both efficacy and safety. There is no clear indication of efficacy of EGFR antibodies in patients with RAS mutation and severe intoxicity may impact a physician’s willingness to prescribe the drug. AFM24 offers a differentiated mode of action functioning through NK-cells.

The EGFR CD16A targeting molecule offers increased potency and compared to cetuximab in NK-cell mediated killing of cells extracting low levels of EGFR results. AFM24 has the potential to address a broad patient population, including patients with resistant to standard of care.

Pilot toxicity studies with our TandAb format has been encouraging and AFM24 showed first evidence of a beneficial profile when [indiscernible] and repeated dose in cynomolgus monkey. Slide 17, shows how AFM24 is differentiated from other therapeutics.

Here you can see that in vitro and in vivo [indiscernible] mediated highly potent tumor cell, killing the tumor versus into EGFR targeting agent. On slide 18, we show you the development of novel multiple tetravalent bispecific antibody in addition to our standards, which has novel bispecific properties.

Final candidate has been selected for AFM24 and as you can see in this example, this novel antibody confers similar of toxicity compared to in vitro in A431 cells. We are currently developing different in R&D making studies in order to identify the ideal candidate with the vast therapeutic window and which is able to address resisting patients.

Slide 19, our second preclinical NK-cell engager program, represented a novel approach to treat multiple myeloma. Key still remains elusive and medical need to achieve minimal residual disease negativity at or shortly after autologous stem cell transplant is not yet addressed.

BCMA is a highly promising novel target based on early clinical data for example from CAR-T and anti-body drug concentrate. Low expression of BCMA is a significant hurdle to eliminate malignant cells.

NK-cells are the first lymphocytes to recover post transplant, which leads us to believe that there might be a significant opportunity to exploit AFM26 in the autologous stem cell transplant setting as known for in combination with adoptive NK cell transfer.

AFM26, which we are investigating a novel tetravalent bispecific antibody formats offers a differentiated mode of action as it binds to BCMA and CD16A with high affinity. The molecule is distinguished from other approaches such as cetuximab and allows targeting of cells expecting very low levels of lysis.

In addition the NK-cells based approach may offer beneficial safety profile competitive. Moreover AFM26, might have a convenience advantage as a novel format is eyeing to compare a significant as a PK profile compared to other.

Slide 20, these data demonstrate that AFM26 can expect killing and kill tumor cells with BCMA expression levels as low as a few hundred receptors per cell. AFM26 mediated tumor cells killing is shown here in different cell lines including the three BCMA low expressing cell lines, the ticks in red.

It has been described that such lines are resisting to killing by BCMA targeting anti-body clinically which may require a larger number of receptors for efficient killing. And this program targeting BCMA may represent a very good factor for developing an NK-cell engagement.

I will now hand over the call 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 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 the Q3 2017 and Q3 2016 are unaudited. Cash and cash equivalents and financial assets totaled €41.8 million as of September 30, 2017, compared to €44.9 million as of December 31, 2016.

Affimed’s operational expenses were primarily offset by net proceeds of €16.4 million from a public offering of common shares in the first quarter and €2.5 million from the drawdown of the second tranche of loan from Silicon Valley Bank.

Net cash used in operating activities was €20.7 million for the nine months ended September 30, 2017, compared to €25.5 million for the nine months ended September 30, 2016.

The decrease was primarily related to lower cash expenditure for research and development in connection with Affimed’s development and collaboration programs and to the expiration of the Amphivena collaboration. Affimed expects to have cash to fund our operations at least until the end of 2018.

This provides runway for the planned development of our clinical program as well as for further discovery and early development activity. Revenue for the third quarter 2017 was €500,000 million compared to €900,000 for the third quarter in 2016.

Revenue in the 2017 period was derived from AbCheck Service while revenue in the 2016 periods relates predominantly to Affimed’s collaboration with Amphivena’s. R&D expenses for the third quarter 2017 were €6 million compared to €8.8 million for the third quarter 2016.

The decrease was primarily related to lower expenses for AFM13 in our discovery and early stage development activities. G&A expenses for the third quarter 2017 were €1.9 million compared to €2.2 million for the third quarter in 2016.

Net loss for the third quarter 2017 was €8.1 million or €0.18 cent per common share compared to a net loss of €10.3 million or €0.31 per common share for the third quarter of 2016. The decrease of operating expenses was partially offset by lower revenue and higher finance cost.

I will now turn the call back over our 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 incumbent clinical and procurement pipeline of NK-cells engagements as well as from our platform. We have leveraged in our lead product AFM 13 for lymphoma initially focusing on Hodgkin’s, setting and allowing the establishment of cost efficient marketing in the 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 T-cell broaden the scientific leadership of our NK-cell platform.

We are expanding the preclinical and clinical activity of our tetravalent bispecific NK-cell engager platform in solid tumors with our preclinical candidate AFM24. In hematological diseases, we intend to leverage additional opportunities for AFM13 and AFM26 for example in combination with adoptive NK-cells to inhibitors or immune activating agent.

We also developed in T-cells engagements and our lead T-cell engager AFM11 is being investigated in two ongoing ALL and NHL trials. AMV564, a T-cell engager derived from our technology platform is in clinical development to Amphivena to treat AML.

In addition as mentioned earlier, moving beyond our development we are developing different tetravalent bispecific antibody formats, tailored to specific indications inside.

And as outlined in previous earnings calls, we have more projects ongoing at the discovery stage and preclinical including molecules developed from our MHC [ph] type complex targeted platform. Thanks very much. Thank you very much for your interest. The call is now open to questions..

[Operator Instructions] And now we’ll take our first person from the queue Maury Raycroft from Jefferies. Please go ahead your line is now open..

Hi, good morning. Congrats on the progress. For the first question, I'm wondering for the metabolic PRs and CR that you’re seeing with the AMF13 plus KEYTRUDA combo.

Can you contextualize those results? Are they on track with your expectations? And do you think you're getting enough NK-cell activity at the highest does?.

I mean, in the mean time yes, they are in line with our expectations because we're only seeing responses, even if it’s only three patients that is what we're expecting to happen either increase PR on CR rate. So, these are the two positive outcomes in our minds.

Having only three patients is yet far too early if we’re really on track, so that we’re analyzing the patients and it actually should have a better picture on that. But overall, the data are encouraging because you can see a very minimum trend from the lowest to the highest dose of AFM13..

Got it.

And do you have a sense of the NK-cell activity that you're getting with the different doses, do you see some, a dose response with that?.

As I say, yes, so with three patients in these cohort, I think it's not possible to make a judgment and so we haven’t analyzed the things in vivo to date. But I hope that we can present more of that during our ASH presentation..

Okay.

And for the responses, are those confirmed and what type of follow-up data will we see at ASH and I guess, I think you mentioned the follow-up will go after three months?.

So, indeed the study is designed that patients are treated are until they relapse. So, that means that will have to have data that look out into the very distant future.

So, obviously we’re collecting the three months data is our first endpoint, this will run into six months data and eventually we’re going to have duration of the durability of response data that just will take awhile. What we are currently doing is we have expanded the dose expansion cohort so we are enrolling patients.

And eventually we’re going to see data from over 20 patients treated at the highest dose cohorts. So, that means that we’ll have a connection of different time points where we measure, at three and six months and then we’ll also have the durability of response.

Initially data however looked quite – as I said, it looked quite encouraging and we'll see on want we can present during the ASH..

Got it. Okay. Then for the AFM13, complete response you’re seeing within the cutaneous lesion.

What's the time schedule for the serial biopsies? Can you comment on the changes and infiltrating immune cells and/or decreasing cancer cells that you observed in this patient over time?.

And so kind of giving an answer on the last one, this is an ongoing study and very reasonable, so that we are trying to raise the times the readout of the translational work hasn’t been done yet, so that is still ongoing.

In terms of zero biopsy, so we treat the patients over eight weeks and we have upto five time points when these biopsies can be taken. In this case as we have seen already a very substantial response within the first three weeks, we only have a limited opportunity to take these samples.

So, overall, as basically what we would do, is we will take a biopsy after eight weeks also and this first patient that hasn’t been possible. So, you do three-dose, first dose and then within the first weeks and then at the end of the treatment. This is how the schedule works..

Got it.

Can you comment on how many patients you have enrolled in that study? And when we could see a data from those patients?.

In terms of enrollment, we have enrolled the first – so what we're doing is we're doing three different dose levels, currently that's the 1.5 dose level. We will then have a higher dose level and this was given once weekly in this first cohort and with our three patients in each dose first cohort.

We can however, also decide this item in the study and enroll more patients. Currently, the first cohort has been fully enrolled and patients are currently being treated. So, the only patient that we have analyzed is the first one..

Got it. Okay, thank you very much and I’ll hop back in the queue. Thank you..

Thank you..

And now we’ll take our next question from the queue, Do Kim from BMO Capital Markets. Please go ahead. Your line is now open..

Hi, thanks for taking my question. First, on the combo study of AFM13 plus KEYTRUDA. Could you provide a little more detail on the responses that you're observing.

What was generally the time to response and whether the partial responses that you saw were improving at the time of assessment? And can it possibly come CRs over time?.

So frankly, we have not analyzed these datas with that detail. As I said, we’re working on that to have this presented during ASH. So, in that context I cannot yet give you any answers to your questions..

Okay. And responses that you saw in cohort two.

Does that align with AFM13 being a therapeutic dose?.

Correct. So, the dose cohort was below the effective dose of AFM13 cohorts two and three are dose at the low and the high end of our effective dose. So, currently we're seeing that seemingly a higher dose can have a better effect, that's what we have seen in the past also..

Got it, got it. And on the patient with the complete response with the cutaneous manifestation.

Could you provide a little more detail on the history of the patient, whether they've had higher therapies, how long with the duration of their disease was?.

Yeah, it’s a very good question, so I don't have those details at hand here. So, we may be able to do this in a follow-up call or once we present the data. But as we said, this is a patient that has anaplastic large-cell lymphoma.

Has been CD30 positive and definitely the patient has had several pre-treatments and that just send the other details and we're super excited to see this response, but we’re really very super excited to see that the patients already been responding within a couple of days.

And or let's say three days, so this speaks to what we have been reiterating with NK-cell activity can be quite quick. And that's been very important data point for us to see if it’s really happening..

Fantastic, yeah, and just one final question.

Did patient show any treatment related side effects, any infusion related?.

So, in that context, nothing that is reportable, so that means that it will happen then we’ll see on the grade one and grade two. We have reported that also in the combo. So, patient these are the outcome, IRRs for that and is something they can – that wouldn’t hinger international the treatment.

So, to date, we have not seen any impacts IRRs on the treatment of the patients..

Great. Thanks for taking my questions. And congrats on progress..

Thanks a lot, Do..

Thank you. And now we take our next person from the queue, Tim from Wells Fargo. Please go ahead. Your line is now open..

Good morning, it’s Nick on for Jim this morning. First question, Adi, just going back to the combination trial. Did these patients have measurable lesions a baseline? And well, that's the first question..

What do you mean by measurable lesion? Obviously –.

Well, in terms of these [indiscernible] reporting metabolic responses as opposed to recess defined shrinkage of a measurable –.

That used to be endpoint, that in mentioned. So, these are new criteria, the lugano [ph] criteria that are in place. And that explains it so, yes, they do have lesions and, but important to measuring the lesions as the activity was in the lesions, because in some cases we're seeing lesions being still there.

However, there is no activity anymore in the lesions, that's why it’s called metabolic respond..

Okay..

It's not [indiscernible] its lugano criteria that are in function..

Okay. Well, thank you educating me there. And in terms of the patients that had a partial or a complete metabolic response.

Have any of those patients progressed?.

Again, we may show this at ASH in that context, but as we say, unfortunately, I don't have the data at hand. We know that these patients are continue to preset for three months data, so many have come back for the six months data points, but it’s too premature for me to give you a good answer yet..

Okay.

And I know that German Hodgkin Study Group trial obviously they have access to the data, but do you have the ability to sort of compare the responses, so you can try to assess what benefit you're getting from KEYTRUDA?.

So, in terms of doing it, it would require us to do biopsies and they are very rarely employed in the Hodgkin’s Lymphoma setting. So there are not many patients willing to accept the biopsy. This is, however, different strategic positive lymphoma with cutaneous manifestation.

And this may be a much better indication and to give an answer on that question because here you can easy access biopsies, and not the single one, but several one. So, in that context it will be individualized if we would do that, so in comparing data from one study to the other one is, always a little bit critical.

So, we rather would want to do that in the positive lymphoma setting..

So, just remind me for the German Hodgkin, will they report Lugano criteria and of those levels you’re evaluating in the combo.

What dose level are they assessing?.

So the German Hodgkin Study Group is done at seven and the KEYTRUDA study is done at seven. Difference however is that after the first eight weeks the protocol is slightly different. Meaning that in the German Hodgkin Study Group we exactly repeat the first eight weeks by a second cycle.

While with KEYTRUDA after one cycle we’ve continued to co-dose with KEYTRUDA every three weeks. So, the studies are identical in terms of dose levels identical in the first eight weeks, but thereafter, they are slightly different.

So, as that the German Hodgkin Study Group consists of redo the same cycle, again while the combo study we’re giving it every three weeks in combination with KEYTRUDA, it’s more like a maintenance setting and the combo setting..

Okay. And then in terms of the new candidates AFM24 and AFM26, I think your comment was you’re looking for a – what is the best therapeutic window you can achieve with one of the candidate molecules. But you’ve already shown that 24 TandAbs has a much better therapeutic index than cetuximab.

So, what are the key criteria you’re looking for? What is the timing on picking an IND candidate?.

Yeah. So, the background of AMF24 and looking on how patients are treated would require a drug that is ideally given, once we treat or let’s say twice per month. So, that would require us and that’s frequent dosing as we may have to do it for TandAb. So, it's not clear how TandAb dosing is best done.

You may recall we’re doing three times per week for the first two weeks and then we’ve continued to do it once weekly. And that's been the reason why we have been developing the novel platform that has a much better PK profile. We’re currently comparing these molecules because they have different biologic features.

And you're right the AFM24 molecule looks very encouraging. And however, we were saying, if we have a molecule that has even longer half life but has similar features, why wouldn’t we pick that. And that’s the stage we’re in. So, we are comparing the AMF24 turned upwards AMF24 immune structure. And eventually we can be decide, which one to take forward.

There's a lot of biology we have done with these molecules and I can’t if you time on what we’ll have an IND filed, but we’re not engineering anymore. So, that means that we have identified the final candidate and we are comparing that IND that is hence, we already have initiated the line generation.

But as of date, to come back with exact lines we have to differ assessments before we can divide on what’s the real development candidate.

That its novel platform comes back with a very similar content even the superior kind of toxicity to a TandAb, it's been crucially important to really pick up these cells that have these very low very low timings pressures because part of resistant mechanisms of certain blood its simply that you cannot eliminate the full set of malignant cells and you may select especially those that have very low target numbers.

This is something where we can dime in, we have shown it in now in our our presentation. It’s true for CD30. It's true for EPF receptor, but it’s also true for BCMA, which seems to be a really challenging one in that context.

I mean, we are seeing differences of our molecules versus other antibodies, so there is something where our technology has a significant impact. And there's novel structure help us to optimize that..

Okay. Excellent. Thanks Adi. I look forward to the follow-up at ASH..

Thank you, Nick..

And now we’ll take our next person from the queue, Peter Lawson from Suntrust Robinson Humphrey. Please go ahead. Your line is now open..

Adi, thanks for the kind of the fresh data. I mean, so it sounds like the ASH account yet and it sounds like we're probably going to get, I see we’re pretty kind of data. Can you give us any color around what you're expecting to include in a number of patients like the follow-up time or any color around that would be appreciated..

As I had say, I’d rather let that go until we have the data finished for ASH. Most of it is already in the works, we’re sorting it out. Further analysis are done, and you may know, in some settings we have to go back and do certain confirmations we decide. So, we're in the cleaning up process in that context.

And I think that we can have a very strong closure at ASH..

Got you. Thank you. And then the CD30 Lymphoma, the CR you talked about in the press release. You mentioned a cutaneous lesions that was in complete response. Was that for the overall patient as well, were they in complete response for their additional lymphomas. It was just a little bit confusing by the language..

So, the patient obviously have cutaneous lesions and systemic evaluations. It’s a patient with the T-cell lymphoma and eventually growth have to be done and we have to just been able to conclude the assessment of all cutaneous lesions we have that are still ongoing. And the patients are also further treated by the way.

So, what we have seen and that's been very encouraging by the data that we have visible response in a patient that has several lesions at different times parts of the body. And all these lesions were removed. So, this shows us that A; our drug can act in the skin, so it's time to get set and can have a very deep meaningful response.

So, that’s how far we have concluded..

Got you. Thank you.

And then, AFM11, when would we see the dose escalation data for that drug and is it still on pace for first half 2018 or is that too early?.

It’s very challenging to predict indeed because have, as we said, we are in the third, fourth dose levels, according to what we have seen by in vitro data. We are approaching at those levels, so with every dose level that we are approaching and treating patients, we may see the activity.

Just impossible for us to predict if it is the fifth or if it is the seventh dose level, so we feel that we come to proximity of certain – of the activity of eight and 11 but to date we’re still escalating and see that we can achieve that..

Great. Okay. Thanks so much. As you may recall, T-cell engagers, do indeed have a very narrow therapeutic window. So, it's known that T-cell engagers don’t show activity up until the point where they're really active. And then you may be able to at one more dose level.

So, this the challenge that the therapeutic window of these T-cell engagers, isn’t giving you any early in productivity, let me tell this way. It either works, or it doesn’t work, there’s not much in between..

Perfect. Thank you. That’s clear..

[Operator Instructions] We’ll take our next person, Yale Jen from Laidlaw & Company. Please go ahead. Your line is now open..

Good morning and thanks for taking the questions. Just let's start with the combo study that after the third cohort, the dose escalating cohort, you have additional I guess, up to 20 patients.

Could you give us a little bit of update in terms of the recruitment for that part and are those mostly treated with a high dose instead of a low therapeutic effective does..

Yes, our recruitment is ongoing and we're making good progress and indeed yes, it is the highest dose that we’re using for our AFM13 with standard dose of KEYTRUDA..

And should we anticipate for example, updates sometime in 2018, maybe the first half or the second half? Or how should we sort of anticipate the data set after the ASH?.

What we will do is until, so at the time when recruitment of dose cohort expansion is complete, Will can inform you. And then that gives us, the opportunity to talk about the exact timelines..

Okay. Great. And last question here is about the Columbia Study and AOCC on the first patients of data.

In total how many patients you may have mentioned already that to be sort of recruited for this study? And you say that there is couple of doses and what’s the other two doses is planted for this?.

Yeah, so the doses, we haven’t yet mentioned it, but they are all on active dose, so were also because it’s a translational study. We can analyze the implant of NK-cell dosing on NK-cell activation. Currently, we do not want to have that shared in detail.

However, we will have a minimum of nine patients in this study and depends on the results we can go and then the study. consequently just two more patients. So, if they come back very encouraging, obviously it makes a lot of sense for us to spend more time and efforts on the lymphoma piece.

But it is very important because for the longest time we have been treating the Hodgkin patients, which indeed represent a good population because they have high number of CD30 expression.

But the CD30, positive lymphoma is not only widening the opportunities, but it may also give us the opportunity to really deal with patients at different levels with CD30 secrecy and see how important CD30 expression is to the efficacy of our drugs.

And as we’ve postulated here, our drug seem to work well on cells that have low target expressions, so that could be again, something quite exciting for us that we are investigating in the CD30 positive lymphoma field..

And maybe the last question on this one, which is that, the patient you report here and then the picture here, which is I mean, has the tumor removed pretty well on day 21. Does this patient continue to maintain this status or was that – he or she had been relapsed after the later point of the assessment..

Yeah, it’s a very good. Treatment is ongoing. We are – well, presently this is an ongoing study and we only have access to data at certain time point. So, at the moment I can’t give you an answer on your question..

Okay. Thanks a lot. And congrats on the progress..

Thanks a lot..

Thank you. So, ladies and gentlemen, with that we conclude our Q&A session. As there are no further questions, I would like to had the call back to our host for any additional or closing remarks..

Thanks a lot for listening to our earnings call. You’re seeing we are making a good progress with our NK-cell engagers understanding that where the opportunities are.

Engineering high affinities to CD16A seems to very important and is highly differentiating and now combined within the structure Can be about molecules that we intend to develop in our solid tumors and the multiple myeloma. But this is a novel field and we’re dedicated to it and at the moment we are very pleased with our progress.

That we’re all seeing with AFM13 demonstrating to us that there's a preclinical activity in patients that otherwise has no options already have increase with that. Thanks a lot for listening and I look forward to all your right directions, seeing your probably soon at ASH..

Thank you. So, ladies and gentlemen, that will now conclude today's Affimed third quarter 2017 earnings call. Thank you for participation. You may now disconnect..