Adi Hoess - CEO Florian Fischer - CFO.

Brian Abraham - Jefferies Michael Schmidt - Leerink Partners Christopher Marai - Oppenheimer.

Good day and welcome to the Affimed Third Quarter 2015 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 Adi Hoess. Please go ahead..

Thank you very much. I'd like to welcome you to our investor and analyst call on the Q3 financial results.

Before I start the corporate update and comment on the financial results, 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. Slide 3. Our mission is to transforming immuno-oncology using next generation immune cell engagement. We have an unencumbered clinical and preclinical stage pipeline based on bispecific and trispecific TandAb antibodies.

We are applying our platforms to two distinct type of immune cells namely natural killer cells, or NK-Cells, and T-Cells. Our approach to redirect natural killer cells is unique in the industry and we intend to leverage this approach as both standalone and combination therapies.

Since our IPO in September 2014, we raised about $119 million in gross proceeds and our cash position is approximately €79 million including a recent private placement from Aeris Capital. We employ about 40 people with headquarters in Heidelberg and now offices in New York and Boston. Slide 4, here are the recent highlight summarized.

We raised $21.8 million, €19.1 million through the sales of about 3.3 million shares to Aeris Capital, a long-term existing shareholder.

Based on the proceeds received from the sale, the company’s cash position is expected to fund operations including chemical and further discovery and early development activities, at least until the first quarter of 2018.

Next, following acceptance of the company’s proposed protocol amendment, patient enrolment continued into the Phase 1 study of AFM11 in non-Hodgkin lymphoma in October. The new protocol as we reported last time allowed for investigation of less frequent dosing of AFM11.

We further have presented first data at the Annual SITC Conference on the company’s proprietary T-Cells and in K-Cell TandAb generated against the tumor specific variant III of Epidermal Growth Factor Receptor. The molecules AFM21 and AFM22 show similar cytotoxic and in vitro potency.

The company anticipates final candidate selection and initiation of IND-enabling studies in the first half of 2016. We will further present two abstracts as post the presentations on further preclinical work at the upcoming ASH meeting. Affimed is a global leader in natural killer cells based immuno-oncology approaches.

As such we believe that AFM13 is the most advanced NK-Cell engaging antibody in clinical development. This bispecific TandAb attaches to both cells and thereby brings immune cells into proximity to tumor cells leading to activation of natural killer cells and perhaps even killing of the tumor cells.

AFM13 indeed demonstrated a clinical pharmoco-dynamic activity in heavily pre-treated Hodgkin lymphoma patients. Furthermore, it showed a very good safety profile and hence we believe it to be well suited for combination with a wide range of other drugs. AFM13 is currently in Phase 2A study and we expect to record data throughout 2015.

To enhance our leadership in this space, we are developing further natural killer cell engaging TandAbs that are expected to enter R&D enabling studies in 2016. Slide 6. We now understand that natural killer cells are very potent killers of cancer cells and the gatekeeper of adaptive immunity.

Indeed NK-Cells represents the most prevalent pathway by which tumors evade the immune system. However, once engaged natural killer cells can ignite the entire immune cascade beginning with antigerm presentation and leading to T-Cell activation.

This destruction of tumor cells by natural killer cells leads to the release of cytokines, very specific cytokines and antigens, followed the antigens presentation to T-Cells. Hence NK-Cells play a key role in stimulating the adaptive immune response.

In order to engage NK-Cells Affimed generated a specific antibody directed against CD16A, which we believe is the most potent known on/off switch on natural killer cells.

This approach is unique in the industry and could potentially become a second cornerstone of novel therapies in addition to T-Cell direction through CD-3, an approach pursued by several other different companies.

Interestingly the activation of natural killer cells is similar to T-Cells modulated by a balance of activating an inhibitory pathway, which is indeed of significant interest to the industry. While current approaches modulate the activity of those lymphocytes that exist in the tumor these approaches cannot redirect.

This is why our approach is very well differentiated. TandAb redirect natural killer cells to the tumor and increase the number of NK-Cells within the tumor and subsequently the T-Cells activated. Slide 8, our lead drug, AFM13 is the clinically most advanced NK-Cell engager to-date.

We are developing it as a potential therapy for CD30 positive lymphoma and equally important we believe it will validate the natural killer cell platform in a broader scope. AFM13 was well tolerated and demonstrated clinical and pharmacodynamic activity in heavily pretreated Hodgkin lymphoma patients.

We are currently running a Phase 2a study of monotherapy within optimized regimen and a much longer treatment period. In preclinical experiment, we most recently have shown that AFM13 acts in synergy with checkpoint modulators and furthermore was able to increase T-Cell infiltration in the tumor micro environment.

Slide 9, I mentioned before that we investigated the potential synergy of AFM13 with checkpoints inhibitor. Efficacy was assessed by in vitro cytotoxicity and in patient derived xenograf in vivo models with AFM13. Anti CTLA-4 and PD-1 and anti-CD-137 antibody. These studies were performed at the Stanford University and we showed the data at ASCO.

We could show that in vivo synergy of AFM13 and checkpoint inhibitors in combination was observed and what’s most impressive for the combinations of AFM13 was PD-1.

Slide 10, we believe that our natural killer cells TandAb platform and in particular our first NK-Cell based product AFM13 has the potential to become a transformative approach to treat cancer. AFM13 is the only CD-16A specifically the 16A targeting bispecific antibody in clinical development.

It distinguishes between natural killer cells and neutrophils. It redirects NK-Cells to the tumor and it has patent protection at least until 2026. AFM13 is also the only tetravalent bispecific molecule in clinical development. The tetravalent instructor of our TandAbs with four binding sites enables dual binding to both tumor and immune cells.

The resulting avidity effect generates 10 to 100 stronger binding to both cells resulting in higher potency. AFM13 is also the only NK-Cell platform currently available for commercial viable bispecifics. TandAbs are single gene constructs that deliver products with a homogeneity greater than 97%, which is critically important for commercial material.

TandAbs in contrast to other bispecific immune-cell engager platforms are not cleared by the kidney and their resulting longer half-life enables convenient IV dosing.

Slide 11, AFM13 is a drug with the potential to be a [safe] and more efficacious treatment for CD30 positive malignancies and we believe that it will also validate the CD-16A natural killer cells platform for applications to solid tumor indication.

As mentioned before, AFM13 currently is the only specific NK-Cell engager in the clinic increasing natural killer cell tumor penetration. This approach has the potential to restore the anti-immune cascade for a more robust and lasting fight against cancer cells.

To-date the NK-Cell approach has demonstrated impressive safety, no cytokine release syndrome, with no MTD reached in the AFM13 Phase I study. Very importantly, our clinical development approach has been broadened and we’re creating an opportunity for mono and combination therapies.

In terms of milestones, we are planning to report stage one data of the monotherapy in Hodgkin lymphoma in the first half of 2016. We further plan to initiate a combination study of AFM13 with PD-1 in the first-half of 2016 in Hodgkin lymphoma.

Based on our preclinical data, this clinical work is of high interest drug as we believe that in addition to natural killer cells tumour infiltration, cytotoxic [T-Cell] infiltration might also be enhanced through AFM13.

Proving this in the clinical setting will position our NK-Cells platform as being widely applicable to tumors to enhance efficacy of PD-1 or even to demonstrate efficacy where PD-1 until now has shown limited effects. We plan to record data in late 2016 on the aspect.

A third study is the Phase Ib/2a IST in CD30 positive lymphoma that could broaden the market potential. In addition this study is designed to enable multiple biopsies and we will thereby gain critical insight into recruitment of NK-Cells into the tumor over time.

This trial and additional preclinical work will enable us to better understand NK-Cell efficacy in the tumor environment and its influence on the adaptive immune system. Slide 12, we have been generating further NK-Cells engagers for solid tumor indications.

Earlier this month, we represented data at SITC that the NK-Cell TandAbs AFM22 that recognizes EGF receptor variant III and CD16A shows similar potency as AFM21 [T-Cell TandAbs] variant against EGF receptor variant III. We intend to select either AFM21 or 22 for further preclinical development and to initiate IND enabling studies in 2016.

We have been generating additional natural killer cells engaging molecules for the therapy of colon and lung cancers as well as for multiple myeloma. In addition to our unique position in NK-Cell based cancer immunotherapy, Affimed is also one of the leaders in the T-Cells recruitment phase, a highly potent approach to eliminate tumor cells.

For T-Cells based approaches, it is important to note that conventional antibodies cannot overcome the tumor cells escape mechanism via T-Cell engagement because T-Cells lack anti-gamma receptors.

Hence other options are required for specific T-Cell engagements and are currently being pursued with a variety of approaches, including bispecific antibodies, T-Cells and other cell based platforms. Efficacy with bispecific T-Cell engagers has been demonstrated in blood cancers and the first T-Cell engager has now been approved in the U.S.

for the treatment of ALL and has received conditional approval in the EU. Other promising data have been published showing effect in blood cancers. However, all data is at a fairly early stage.

Important were the report, the side effects needed to be carefully managed and the bispecific T-Cell approach in ALL showed that interruption of dosing was an effective way of resolving critical issues. Overall convenience and cost remain key issues.

The most advanced molecule for T-Cell engagement is Blincyto, a CD-19, CD3 bivalent BiTE molecule approved in the U.S. and conditionally approved in the EU for the treatment of ALL. Our lead candidate AFM11, a tetravalent CD19, CD3 molecule has been developed as a potential competitor to Blincyto.

AFM11 has a differentiating target product profile, which we believe has advantages over Blincyto. In 2014, we initiated a Phase I dose escalation in NHL, ALL patients with an intensive dosing regimen. However in August, we amended the Phase 1 protocol optimizing their regimen to a less frequent dosing.

In addition, we have split the NHL and ALL indications into two separate studies within the Phase I allowing differentiation for the ALL indication. The revised protocol has been accepted and patient enrolment continues into the Phase 1 study of AFM11 in NHL in October. We expect first data to be available in the second half of 2016.

We have already reported on our partnerships with Amphivena and Janssen and now I want to move to Slide 17, where our pipeline summarize. So we have five pipeline programs directed against CD13, CD19, EGF receptor variant III, CD33 and multiple myeloma targets.

Our NK-Cell engager, AFM13, will be investigated in three clinical studies as reported before. For AFM11 we have made an important adjustment to our clinical development strategy as we are now testing a much less frequent dosing regimen in NHL.

In addition the ALL indication will now be pursued in parallel offering a second therapeutic option in addition to non-Hodgkin lymphoma. Our third program is targeting EGF receptor variant III bearing tumors.

With this program we now have the unique opportunity to compare NK-Cell and T-Cell engagement side-by-side for their application to solid tumor, with our TandAb AFM21 and AFM22. The fourth program is investigating T-Cells TandAb directed against CD33 and developed in AML.

Our trispecific antibody approach takes advantage of the four domain nature of our platform allowing the generation of multi-specific antibodies. Our initial goal is to generate trispecific antibodies that recognize two different cancer cell antigens in addition to an effective cell antigen.

This could result in high affinity and importantly increased selectivity for malignant tissues as compared to healthy tissues.

This platform would offer an expansion to the target space critically issued for T-Cells engagement for the selective targeting of tumor cells versus healthy cells and we have initiated a discovery program for the therapy of multiple myeloma. Affimed plans to have significant news flow over the next 18 months on all its programs.

We intend to provide an update on the monotherapy of AFM13 in Hodgkin patients in the first half of 2016. We’re also working on the initiation of [IHC] and the translation study of AFM13 in CD30 positive lymphoma patients and in combination with PD-1 in Hodgkin lymphoma patients.

We further will provide an update at Ash on preclinical data on AFM13 in combination with checkpoint inhibitor. For AFM11 appropriate update is in the second half of 2016. For our EGF receptor variant III program, we intend to select the development candidate to our enabling studies in 2016 with a potential IND filing in 2017.

For the CD33 collaboration program with Amphivena/Janssen we are currently performing [indiscernible]. In discovery, we are currently focus to generating further candidates either based on bispecific or trispecific platforms. I will now hand over the call to Florian Fischer, our CFO 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.

The financial results for the third quarter 2014 and for the nine months ended September 30, 2014 include certain non-operational and non-monetary effects, due to our corporate reorganization in connection with our IPO in September 2014.

Our consolidated statement of comprehensive income and loss for the third quarter 2014 was largely effected by the change of the estimated fair value of our share-based payment awards.

In addition our preferred shares were classified as liability prior to our corporate reorganization in connection with our IPO and thus had to be measured by the fair market value. As of the closing of the IPO and the completion of our reorganization, we do not expect any material remeasurement effect in the future.

Additional information regarding these results is included in the notes to the consolidated financial statement as of September 30, 2015 and the management’s discussion and analysis of financial conditions and results of the operations, MD&A which are included in Affimed's Form 6-K as filed with the SEC earlier today.

Cash position, cash and cash equivalents totalled €60.4 million on September 30, 2015 compared to €39.7 million on December 31, 2014 and excludes the net proceeds from the €19.1 million related to the October project placement by Aeris Capital.

The increase in September 30, 2015 cash was primarily attributable to Affimed's public offering of common shares in May 2015. Net cash used in operating activities for the nine months ended September 30, 2015 was €14.5 million compared to net cash used in operating activities of €5.1 million for the nine months ended September 30, 2014.

The increase was primarily related to the increase in cash based expenses for R&D in connection with our development and collaboration programs and G&A expenses in relation to our operations as a public company. Affimed expects to have cash to fund our operations at least until the third quarter 2018.

This provides run rate for the client development, of our clinical programs, as well as our further discovery and early development activity.

Revenue for the third quarter 2015 was 1.2 million and 5.9 million for the nine months end of September 30, 2015 compared to 1.9 million for the third quarter 2014 and €3.3 million for the nine months ended September 30, 2014.

Revenue is primarily attributable to the two collaborations with Amphivena and [indiscernible] and is related to the respective project progress.

Research and development expenses for the third quarter 2015 were 6.4 million and 15.0 million for the nine months ended September 30, 2015 compared to €2.2 million for the third quarter 2014 and €5.5 million for the nine months end of September 30, 2014. The 2014 R&D costs were largely affected by non-monetary effect.

Since our reorganization in September 2014 these effects have not appeared again. The increase in end expenses primarily related to the advance majority of the preclinical and clinical development program and the broadening of our preclinical and discovery pipeline.

G&A expenses for the third quarter 2015 were €2.1 million and €5.6 million for the nine months ended September 30, 2015 compared to G&A expenses of €249,000 for the 2014 and 600,000 for the nine months end of September 30, 2014.

G&A expenses for 2014 primarily related to the remeasurement gains due to the change of the estimated fair value of our share based payment awards in 2014 and are also related to legal and auditing expenses and to legal cost associated with our Dutch legal entity formed in connection with our corporate reorganization.

In the 2015 periods, the G&A costs are mainly associated with our operations as a public company.

Net loss for the third quarter 2015 was €7.3 million or €0.24 per common share, and €14.0 million, or €0.52 per common share for the nine months ended September 30, 2015, compared to the net income of 13.3 million or earnings of €0.44 per common share for the third quarter 2014, and an income of €5 million or earnings of €0.32 per common share for the nine months ended September 30, 2014.

The generation of a net income in 2014 is primarily related to the remeasurement gains of share–based payment awards and other non-monitory effect due to the corporate reorganization.

In 2015, the net loss is attributable to the higher expense and revenue ratio associated with our R&D activities and the higher level of G&A expenses related to our operations as a public company. I will now turn the call back over to Adi for summary of our two clinical programs and our pipeline.

Adi?.

Florian, thanks very much and I would like to now open this call for questions please..

Thank you. [Operator Instructions] We will now take our first question from Brian Abraham from Jefferies. Please go ahead..

Thanks for taking my questions.

Starting with AFM13, I wonder if you can take a little bit about what we might look for in the second quarter of next year from the interim Hodgkins data cut in terms of just the degree of follow-up the number of patients approximately that we might initially see data from and whether there is going to be any biomarkers that you will be presenting as well?.

Thanks a lot. So the AFM13 study is conducted in Hodgkin lymphoma that has sales, [indiscernible] treatment mostly fourth line patient, fourth and fifth line patients. What we are measuring here is so as compared to our initial study is again the [indiscernible] response rate after three months and after six months and also [PFS] data.

So that describes the overall concept of this study. And as you may remember in our Phase 1 we have treated patients currently over four weeks and now we have a much stronger treatment period. And objective responses are measured by [testing] criteria of dose that we will assess both changing tumor math and changing metabolic activity.

In state and the primary endpoints is pretty much the objective response rate after three months. So what we intent to report in the first-half of 2016 is objective response data after three months based on roughly 20 patients treated to this time count. In terms of biomarkers to your question, we have a series of biomarkers that we are investigating.

However at the moment there is -- so based on our Phase 1 study, we have not yet identified a very clear biomarker in order either to assess in K-Cell activation that relates to tumor shrinkage. So we have a much broader assessment here, we need to see how much of a correlation we can identify there..

And then on the AFM21 and 22 programs, just wondering if you can talk little bit about what might influence your decision to choose one over the other, sounds like both are looking pretty promising at this stage and is there anything that’s kind of evolving in our understanding of harness in NK-Cells versus T-Cells in the settings that you're planning to move forward with that might guide your decision?.

So in this target it's been reported that T-Cell engagement appears to be more powerful than natural killer cell engagement. So we have seen quite some strong data by the different strategies and obviously there is much fewer data on natural killer cells based approaches.

When we compared historically these molecules again in the last, there's been always a kind of 10 to 20 fold higher potency described for T-Cells and for natural killer cells.

Meaning that the T-Cells approach usually ended up in the low [indiscernible] range, while this natural killer cells based approach was more in the 10 to 20 fold [indiscernible] range. For this molecule, AFM22 is CD16A EGF receptor variant III targeting TandAb this is different.

So we now have engineers TandAb of much higher potency and that difference pretty much disappear. So T-Cell engagement and NK-Cell engagement at least in vitro are looking very comparable.

We know of one advantage of natural killer cells this is that it seems to be favor in the chemical that could be one of our decision criteria why we would favor an NK-Cell engager over a T-Cell engager. And that particular faced the advantage will be used not to just to have a data therapy, but also actually investigate the appropriate combination.

So we’re a great believer of moving into oncology with combination. And it seems at the moment more favorable to move with the natural killer cells based approach than with the T-Cell approach that would affect our definitions..

We will now take our next question from Michael Schmidt from Leerink Partners. Please go ahead..

Thanks for taking my question.

I had one on AFM13, could you speak a bit more about your plans in addressing other lymphoma ties, other [indiscernible] positive lymphoma types beyond Hodgkins?.

So it's been described as CD30 indeed expressed in almost every kind of lymphoma to varying degrees. There are T-Cell lymphoma that are described to express CD30 even above 95% of cases. So this will be [indiscernible] cell lymphoma.

However also contain T-Cell lymphoma have a significant degree or -- significant number of patients it also express CD30. And in addition we have now data that were presented by different groups that show the expression of CD30 in T-Cell lymphoma.

So very likely that the patient number can be expanded by a factor of three to far as compared to Hodgkin lymphoma, so that’s one of the drivers that basically are important for us in order to engage into CD30 positive lymphoma.

In this particular study however, we have a second focus and the second focus is to really understand more details on how engagement works in tumor environment. So we’re indeed focusing on patients that have CD30 positive lymphoma, but in addition have contained [indiscernible] and thereby we can take the [serial point].

So this study really has two important learnings for us; first, how effective can a CD30 directive therapy be outside of Hodgkin lymphoma and secondly, what’s happening in the micro environment looking at natural killer cells and also on specific cytokines on the cytokines [indiscernible] in addition to T-Cell involvement at that point.

That's the driver of that study..

And then for AFM11 regarding the study in ALL, I was wondering if you're including both adult and pediatric patients in that protocol or just one of the two groups?.

So at the moment I cannot yet give you an answer, we’re evaluating that but the likelihood that we will only include [adulation] is very high..

[Operator Instructions] We will now take our next question from Christopher Marai from Oppenheimer. Please go ahead..

Thanks for taking the questions. I was wondering if you could first comment on AFM21, you had a great post direct 50, targeting EGFR variant III is obviously been a bit of validated approach.

How do you look at what potential indications to go into? And does your [indiscernible] format give you any certain advantages with respect to molecular size and [blood brain] barrier crossing or in other indications is really the potency of the molecule going to give you an advantage potentially over the other [indiscernible] approaches? Thanks..

Yes, we have conducted a variety of immuno chemistry experiments with our lead molecules and we’re learning that EGF receptor variant III is indeed expressed in [indiscernible] you are referring to crossing of the blood brain area, but we have also discovered that EGF receptor variant III is expressed in a variety of solid tumor that may include lung and [neck], so we’re currently looking deeper into these indications, these experiments are currently ongoing and as we have said we’re comparing the two molecules 21 and 22 and we’re comparing these also in different preclinical models, animal models in variety of tumors and that will guide us on which indication we finally [made the luck].

What we have learned is that antibodies again variant III may indeed behave quite differently. So when we have done an [ethical message] for our antibody, we discover that for example we have a different [indiscernible] antibody. And having a different [indiscernible] this may also guide us to -- help us to guide the appropriate indications.

So these are minor [indiscernible] major details that we are currently evaluating and that helps us to directly their proper indications. Obviously we are knowing if we’re going to the brain and have a very potent [indiscernible] T-Cell engagement you [may can’t find it].

So we don’t know if the natural killer based approach, again we’ll be here a bit of a strategy, but these topics are currently all being looked at a great detail and we probably can say around [indiscernible] which will be molecules we’re picking and also which of the indications we’re picking.

But just for your information, we don’t have to be decide within the next 18 months or let's say 15 months on a specific indication that’s not required for us. We have the opportunity to broadly pursue this molecule for all specific indications and then can even do a broader Phase 1 study.

So indication at that stage is not a key decision criteria for these molecules for the selection of the molecules..

And then with respect to the AFM13 it seems in the early studies you probably didn’t dose high enough or long enough with that molecule.

I was wondering if you can comment; number one, on dosing and how you distribute your dosing strategy? And number two, how are you measuring the biological half-life of these molecules, I mean my understanding is through your [indiscernible] effect you could actually [indiscernible] tightly to some of these NK-Cells potentially or targeted and as a result be sort of in systemic circulation for much longer than you might be in sort of the plasma.

How are you measuring that and do you think that might provide a strategic [manage] for your approach versus some of the others? Thanks..

Indeed very good question, so this is what we are learning more and more in detail that we may not -- so half-life is very important for drug than drug receptor linked interaction, because you need to have enough drug in the circulation to have a permanent blocking.

Both NK-Cell and T-Cell engagement drug in quantities where we only have a fraction of your receptors really occupied and then the immune starts to fire. So pretty much is sufficient to have anywhere between 10 maybe a 100 molecules second on an immune touching the cancers out and then really activate.

And the total binding side in these maybe in the range of our -- maybe, but are in the range of 10,000 to 100,000. They need much smaller [indiscernible]. So we need to fuse exactly the so called drug half-life versus the pharmacodynamic half-life.

And I cannot speak yet in detail about on the experiments that you're currently performing, but we’re exactly addressing questions that you have raised, how long is the half-life of a [conduct] either attaching to the immune cell or being bounced directly in the tumor environment.

And because we have this tetravalent structure meaning that we always occupy two binding side on each side of the cell we may indeed have very affinity that make the molecules residing within tumors and immune cell for a long time.

In vitro, we already have shown that, so pretty much once our conducts are bound to the respective cells, it's very challenging to really wash them off. So their half-life on the respective cells is indeed quite long..

And do you think, I mean it's a very potent approach retargeting T-Cells, do you think that longer half-life might result in potential safety concerns? And then just finally on CD-19 and AFM11, have you been engaged in any partnering discussions or have you had any incumbent interest on potentially partnering that program, obviously the targets been sought after in the business development growth? Thank you..

So in terms of safety we cannot say anything yet. So we’re in the dose escalation phase and there we haven’t yet announced any data and as a fact this may last another year before we first time talk about the AFM11 safety and efficacy data.

Regarding partnering, our strategy is consistent; we have always said that we do not intent to partner the program.

So one of the reasons for partnering would be that you raise, basically you get non-dilutive cash that you will have to use for other programs, all our other programs are at a very early stage and require limited amounts of cash and as you have seen we have just two findings in this year that helps us to run the company independently or going into partnering discussions.

And we really believe that AFM13 and AFM11 are very strong assets that once we have generated substantial clinical data that have much higher value than what they currently have, especially with AFM13 we are going to dual strategy are pursuing this as a monotherapy and a combination therapy and this would not just validate the drug as a potential therapy for Hodgkin lymphoma but it's also validating the [indiscernible] approach.

Again AFM11 is an approach addressing basically, we have a molecule with CD-19, CD-3 that’s validated by Blincyto, so why should we give it away at that stage with no reason until we have clinical data..

And then just with respect to CD-19 is there any particular sort of niche indication that you see as particular [factor] that potentially bringing this molecule into the clinic on your own? Thank you..

So the niche indicating that you're focusing on with AFM11 at the moment is still non-Hodgkin lymphoma, but it's not a niche..

I apologize, I was referring to the CD-19, my mistake is there any niche indication for the CD-19 molecule, since you're not looking to partnering that?.

So in terms of CD-19 our focus eventually will be not to resell lymphoma that is the indication with the highest need and we haven’t really thought on a niche beyond that particular indication. Thank you..

There are no further questions from the audio at the time..

Okay. Thank you very much for participating in our Q3 financial call. We’re now closing the call. Good bye..

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