Adi Hoess - Chief Executive Officer Martin Treder - Chief Scientific Officer Florian Fischer - Chief Financial Officer Jens-Peter Marschner - Chief Medical Officer.

Chris Howerton - Jefferies.

Good day and welcome to the Affimed Second Quarter 2015 Financial Results and Corporate Conference Call. Today’s call is being recorded. At this time I would like to turn the conference over to Adi Hoess. Please go ahead sir..

Thanks a lot. I would like to welcome you to our investor and analyst call on the second quarter financial results 2015.

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.

Except as required by law, we assume no obligation to update these forward-looking statements publicly, or to update the reasons why actual results did 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 statement regarding forward-looking statements in our Form 6-K filed with the SEC earlier today.

Thank you for your understanding. I will start now the presentation with Slide three. Our mission is to transforming immune-oncology using next generation immune cell engagers. We have an unencumbered clinical and preclinical stage pipeline based on bispecific and trispecific TandAb antibodies.

We are applying our platforms to two distinct types of immune cells namely natural killer cells, or NK-Cells, and T-Cells. Affimed’s approach to redirect NK-Cells is unique in the industry and we intend to leverage this approach as both standalone and combination therapies.

The company has two ongoing partnerships, one with the Leukemia & Lymphoma Society and the second one with Amphivena/Janssen. Since our IPO in September 2014, we raised $97 million in gross proceeds and our cash position is approximately Euro 66 million as of the end of June 30.

We employ about 40 people with headquarters in Hyderabad and now offices in New York City and Boston. Slide 4, we had a number of highlights already this year, especially in the second quarter.

Most importantly in May 2015 we raised about $41 million in gross proceeds in a follow on offering with the objective to broaden our AFM13 and AFM11 clinical programs. In June, the company was added to the Russell 2000 index. For AFM13 we initiated the Phase 2 study recruitment in Hodgkin lymphoma. Here we are testing the drug as monotherapy.

Another highlight were our four poster presentations at ASCO. There we showed that AFM13 has a strong synergy with PD-1 in eliminating human Hodgkin lymphoma tumors in a PDX model in combination studies of AFM13 with checkpoint inhibitors performed at Stanford University.

Four other posters were presented on the collaborative CD30/CD3 program with [Indiscernible]. This program validates the robustness of Affimed's TandAb platform and demonstrated corroborative evidence of direct correlation between binding affinity and potency.

Another milestone has been the establishment of our operations in the United States and the hiring of key personnel for investor relation and clinical development.

We also formalized a Scientific Advisory Board with distinguished members spanning a broad range of areas relevant to Affimed's approach including immuno-oncology, Natural Killer cells, lymphoma and leukemia. Affimed's wholly owned subsidiary, AbCheck, is an important source for our own need of human antibodies.

In addition, AbCheck offers its services to a limited number of third parties, and AbCheck most recently announced the expansion of its ongoing collaboration with Pierre Fabre Pharmaceuticals on human antibody generation.

An absolute highlight for AbCheck was the award at PEGS as "Best Poster" for its novel technology enabling accelerated humanization of rabbit antibodies. This platform is called mass immunization. Slide 5, we are a global leader in natural killer cell based immune-oncology approaches.

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

AFM13 demonstrates a clinical and farm pharmacodynamic activity in heavily pre-treated lymphoma patients. Furthermore, it showed a very good safety profile and hence might be well suited for combination with a wide range of other drugs. AFM13 is currently in Phase 2 and full data are expected in 2016.

Here we are testing AFM13 as monotherapy in Hodgkin lymphoma. To enhance our leadership, we are also developing further NK-Cell engaging TandAbs that are expected to enter R&D enabling studies in 2016. Slide 6, NK-Cells are potent killers of cancer cells and the gatekeeper of adaptive immunity.

Indeed NK-Cells represent the most prevalent pathway by which tumors evade the immune system. However, once engaged NK-Cells can unite the entire immune cascade beginning with [antigerm] presentation and leading to T-Cell activation.

The destruction of tumor cells by NK-Cells leads to the release of cytokines and antigens, which are picked up by macrophages and [Indiscernible] for [antigerm] 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 against CD16A, which we believe is the most potent known on/off switch on NK-Cells.

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

Slide 7, interestingly the activation of NK-Cells is similar to T-Cells modulated by a balance of activating and inhibiting [Indiscernible], which of significant interest to the industry.

Almost all major pharmaceutical companies are running late stage clinical trials with various antibodies, either inhibiting or stimulating T-Cells and NK-Cells such as [CD137], CS-1 or PD-1.

While these antibody approaches can modulate the activity of immune cells, the major benefit of Affimed's approach is that our TandAbs target CD16A, and thereby with the second specificity redirect NK-Cells cells to the tumor cells.

Thereby they bring these cells in close proximity leading to subsequent activation and to the destruction of the tumor cell. Slide 8, our lead drug, AFM13 is the clinically most advanced NK-Cell engager up-to-date.

We are developing it as a potential therapy for CD30 positive lymphoma and equally important we believe it will validate the NK-Cell platform in a broader scope. AFM13 redirects NK-Cells and these become activated only upon binding to the tumor.

It already demonstrated the clinical and pharmacodynamic activity in heavily pretreated Hodgkin lymphoma patients and we are currently running a Phase 2 study as a monotherapy in Hodgkin lymphoma. We believe that the effect can be further maximized by an optimized regimen in a much longer treatment period.

Very importantly, AFM13 showed a very good safety profile in Phase I and might therefore be well suited for a combination with a wide range of other drugs. In preclinical experiments we most recently have shown that AFM13 acts in synergy with checkpoint inhibitors.

Slide 9, I mentioned before that we investigated the potential synergy of AFM13 with checkpoints. Efficacy was assessed by in vitro cytotoxicity and in patient derived xenograf in vivo models with AFM13, and antibody against directed CTLA-4, PD-1 and CD-137. In vivo synergy of AFM13 and checkpoint inhibitors in combination was observed.

In each case, when AFM13 was combined with a checkpoint modulator the efficacy was enhanced. This was most impressive for the combination of AFM13 with PD-1. Furthermore, the efficacy was influenced by the presence of regulatory T-Cells, natural killer cells and cytokines in the tumor microenvironment.

Detailed data were presented at ASCO in May of this year. Slide 10, we believe that our NK-Cell 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 targeting bispecific antibody in clinical development.

It distinguishes between NK-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.

This resulting avidity effect generates 10 to 100 fold stronger binding to both cells resulting in higher potency. AFM13 is the only NK-Cell platform currently available for commercially viable bispecifics.

TandAbs are single gene constructs that deliver products with a homogeneity greater than 97%, which is critically important for commercial grade 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 intravenous 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 NK-Cell platform for applications to solid tumor indication.

As mentioned before, AFM13 currently is the only specific NK-Cell engaged 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.

For example, no CRS, 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 now planning to report stage one data in the first half of 2016, slightly later than initially expected due to a longer than anticipated administrative process to get the Phase 2 started. While we are currently recruiting patients into the Phase II study, we are also well advancing additional opportunities for AFM13.

The Phase Ib/2a study in CD30 positive lymphoma 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.

Furthermore this study will not only investigate AFM13 as monotherapy, but also the combination of AFM13 with PD-1. 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.

We further plan to initiate a combination study of AFM13 with PD-1 in 2016 in Hodgkin lymphoma. Based on our preclinical data this clinical work is of highest interest to us as we believe that in addition to NK-Cell tumor infiltration [cytotech] T-Cell infiltration might also be enhanced through AFM13.

Proving this in the clinical setting will position our NK-Cell 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 effect. Slide 12, as part of our recently raised funding will be applied to further develop NK-Cell engagers in solid tumor indications.

We have discovery programs ongoing for the therapy of lung, glioblastoma, colon, as well as head and neck cancers and multiple myeloma. Our most advanced program there is AFM21, which target EGFRvIII. This is a highly tumor-specific molecule expressed in lung, GBM, and head and neck cancers.

We are currently evaluating both NK-Cell and T-Cell TandAb constructs and we expect to present data on our NK-Cell engager at the SITC annual meeting in November. We most recently presented data on the EGF receptor vIII CD3 TandAb candidates, which have shown efficacy in animal models.

We intend to select a development candidate by year-end to initiate IND-enabling studies in 2016. We are currently generating additional NK-Cell engaging molecule 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 T-Cells recruitment, 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, Chimeric antigen receptor modified 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 recently been approved in the US for the treatment of ALL. Other promising data have been published showing effect in blood cancers. However the data is at a fairly early stage.

Important [Indiscernible], 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 US for the treatment of ALL. Our lead candidate AFM11, a tetravalent CD19, CD3 molecule has been developed for a potential – and has been developed as a potential competitor to Blincyto.

AFM11 has a differentiating TPP, which we believe has advantages over Blincyto. We have developed a robust manufacturing process for AFM11 with very low cost and suitability to be filled [in a vial]. Furthermore, like all our TandAbs AFM11 is tetravalent and due to its avidity effect has a 100 fold higher affinity to CD3.

This results in a much better cytotoxicity at low T-Cell numbers than that have been published for Blincyto. Furthermore AFM11 through its improved half life can be administered by regular IV infusion and thereby overcomes the continuous infusion protocol required for other entities.

We believe that AFM11 is the most advanced T-Cell engager in clinical development in blood cancers next to Blincyto with a well differentiating TPP. In 2014, we initiated a Phase I dose escalation in NHL, ALL patients with an intensive dosing regimen.

However, recent data from competitive programs and our frequent discussions with key opinion leaders, including our newly formed Scientific Advisory Board, have prompted us to revise our clinical development plan. Based on the recommendation of our SAB we have submitted to amend the Phase I protocol, optimizing the regimen to a less frequent dosing.

In addition, we have split the NHL and the ALL indications into separate studies within the Phase I allowing differentiation for the ALL indication. The revised protocol will have an initial impact on the timing of the Phase I completion and we now expect to report data in the second half of 2016.

Nevertheless we are convinced that the revised protocol will enable us to accelerate the overall development of AFM11 and will support the product profile specifically targeted to the evolving treatment landscape.

In summary, AFM11 is well differentiated from competition by its potency and the convenience of its formulation and dosing and we are developing it to meet the therapeutic need, as well as a significant market potential in large indications such as NHL and ALL. Slide 16, we have two ongoing partnerships.

One with Amphivena/Janssen and one with the Leukemia & Lymphoma Society, which provides a major financial contribution to the NK-Cell TandAb AFM13. In our collaboration with Amphivena/Janssen we recently presented the rapid identification of preclinical CD-33 CD3 candidate for therapy of AML.

The lead candidate T564 is stable, highly expressed and displays significant in vitro and in vivo cytoxicity. Our collaborators and affinity presented three posters at ASCO 2015 with collaborative evidence of a direct correlation between binding affinity and potency.

Slide 17, our pipeline comprises of 5 program directed against CD13, CD19, EGFRvIII, CD33 and multiple myeloma targets. Our NK-Cell engager, AFM13, will be investigated as monotherapy and in combination with PD-1 in several CD30 positive lymphoma indications. The majority of data is anticipated to be generated throughout 2016.

The investigation of AFM13 as mono and combination therapy reduces the clinical risk significantly and increases the option for development in [Indiscernible] as well as for front-line therapy.

For AFM11 we have made an important adjustment in our clinical development strategy as we are now testing a much less frequent dosing regimen thereby taking into account the recently published results obtained in competing programs and the implication for AFM11 based on the specific features of our molecule.

In addition, the ALL indication will now be pursued in parallel. Our third program, AFM21 is targeting EGFreceptorvIII bearing tumors. With this program we now have the unique opportunity to compare NK-Cell and T-Cell engagement side by side for the application to solid tumors.

The fourth program, our ongoing collaboration with Amphivena/Janssen is investigating a TandAb directed against CD33 and developed in AML. Our trispecific Abs 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 Abs that recognize two different cancer cell antigens in addition to an [Indiscernible] cell antigen. This could result in high affinity and importantly increased selectivity for malignant issues as compared to healthy tissues.

This platform would offer an expansion of the target space for selective targeting of tumor cells versus healthy cells and we have initiated a discovery program for the therapy of multiple myeloma, for which we also have been awarded a research grant from the German government.

Slide 18, Affimed plans to have significant news flow over the next 18 months on all its programs. We most recently presented exciting initial preclinical data on AFM13 in combination with checkpoint inhibitors at ASCO. We expect to provide a further update at ASH in December.

We further intend to provide an update on the mono therapy of AFM13 in Hodgkin lymphoma patients in the first half of 2016.

We’re also working on the initiation of further clinical and translational studies of AFM13 in CD30 positive lymphoma patients and in combination with PD-1 in Hodgkin lymphoma patients later this year and in early 2016 respectively.

For AFM11 we have submitted an amended clinical protocol with a less frequent dosing regimen in NHL and we’re working on an enhancement of the ALL Phase I study. A progress update for this program is planned in the second half of 2016.

For our AFM21 we intend to compare the preclinical activity of both NK-Cell and T-Cell engagers in parallel and will subsequently select the development candidate for IND-enabling studies. For the CD 33 collaborative program we are currently performing [Indiscernible] we posted at ASCO showing a successful selection of the development candidate.

In discovery, we are currently focusing to generate further candidates truly with a strong focus on NK-Cell engager either base on the bispecific or the trispecific platforms. 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 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 second quarter 2014 include certain non-operational and non-monetary effects, product [Indiscernible] in connection with our IPO on September 2014.

Our consolidated statement of comprehensive income and loss for the second 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 of the completion of our reorganization we do not expect any material remeasurement effect in the future.

Additional information regarding this result is included in the notes of the consolidated financial statements as of June 30, 2015 as a management’s discussion and analysis of financial conditions and results of operations, which are included in Affimed's Form 6-K as filed with the SEC earlier today.

Cash and cash equivalents totaled euros 66.3 million on June 30, 2015 compared to euros 39.7 million on December 31, 2014. The increase in the first half 2015 cash was primarily attributable to Affimed's public offering of common shares in May 2015.

Net cash used in operating activities for the first half of 2015 was euros 7.8 million compared to a net cash used in operating activities of euros 3.5 million for the first half in 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.

The company’s cash position is expected to fund operations including clinical development and further discovery and preclinical development activities into the third quarter in 2017.

Revenue for the second quarter of 2015 was euros 2.2 million and euros 4.7 for the first half 2015 compared to euros 0.7 million for the second quarter of 2014 and euros 1.4 million for the first half of 2014. The revenue is primarily attributable to the collaborations with Amphivena and LLS respectively.

The payments are related to the respective project programs. The milestone payments in the second quarter 2015 and first half 2015 we will cover later at more extensive development periods.

Research and development expenses for the second quarter 2015 were euros 5.6 million and euros 8.5 million for the first half of 2015 compared to euros 2.1 million for the second quarter 2014 and euros 3.3 million in the first half 2014.

The increase is primarily related to the maturity of the development programs and the associated costs for those activities, including any preclinical and discovery activities. The 2014 R&D costs were largely affected by non-monetary. Since our reorganization in September 2014 these effects have not appeared again.

G&A expenses for the second quarter 2015 were euros 1.7 million and euros 3.5 million in the first half of 2015 compared to a credit to the G&A expenses of euros 4.4 million for the second quarter 2014, and G&A expenses of 351,000 for the first half 2014.

The increase was 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 for the corporation of our initial public offering and for legal costs associated with the formation of our Dutch legal entity formed in connection with our corporate reorganization.

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

Net loss for the second quarter 2015 was euros 5.2 million or euros 0.19 per common share, and euros 6.7 million, or euros 0.26 per common share, compared to the net income of euros 13.4 million or euros 0.19 per common share for the second quarter 2014, and a net loss of euros 2.3 million or euros 0.15 per common share for the first half 2014.

The generation of net income in 2014 is primarily related to the remeasurement gains of share–based payment awards. In 2015, net loss is attributable to the higher expense and revenue ratio associated with the 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 an update on our development strategy.

Adi?.

Thank you very much Florian. Our strategy is to maximize the value creation represented by our pipeline and platforms, while leveraging our lead program, AFM13, to establish and marketing key indications.

We are therefore initially focusing on the Hodgkin lymphoma [Indiscernible] enabling us development paths and allowing the establishment of a cost efficient marketing and sales structure. In addition investigating AFM13 both as monotherapy and in combination with PD-1 reduces its development risk and write the application of NK-cell to solid tumors.

Overall, our pre-clinic and clinical strategy is designed to prom the scientific leadership of our unique [CASAL] platform. Another corner stone of our strategy is to use our pipeline and technologies to create value through both next generation product and deal opportunities.

With AFM11, we have an advanced molecule in development in the [indiscernible] engagement space to stat this proof of concept in non-Hodgkin lymphoma and ALL. With the NK-cell platform, we’ve a unique approach to recruit immune zone and its application to solid tumors.

We’re currently generating an advancing each [year percepta varian] 3 and other CD16A in [indiscernible] and solid tumors such as glioblastoma, lung, head and neck, colon and multiple myeloma. In addition we may plan to add value by forming a high value technology platform partnership within industry.

Overall, we believe that Affimed is well positioned in the emerging space of immune-oncology with industry leadership NK-cell based approaches. Thanks a lot for your interest, the call is now open for questions..

[Operator Instructions] We will now take our first question from Michael [indiscernible] please go ahead sir, your line is open..

Hi, good morning and thanks for taking my questions.

I had one on AFM13, I think you already reported a slower administrative process when starting the study last year and I was wondering if you have some more information or granularity on what’s going there on the administrative type of this trial?.

Hi Michael. So, the first part of this news is that we’re recruiting and have patients enrolling. However, unfortunately the process until we could open this first taking considerate long initially when we anticipated as we needed to get several approvals both from regulatory agencies, AFIX committees and also the site initiation.

We’re for the first time here also working together with German Hodgkin study group which is a well established group in the field of Hodgkin lymphoma and we probably also overestimated their speed in order to get this trial set up, as I said, it’s taking about six months longer than we originally thought that we’ve now completed everything and are treatment patients..

Okay, great, thanks.

And for the planned PD1 combination trial can you talk about your strategic thoughts there? Are you planning to do that alone or potentially part of some sort of a collaboration agreement?.

Thanks for that question. So, the most important strategy that we pursue is that we would want to want – that we intend to control this study from the Affimed side.

We are open for a partnership that a third party is providing PD1 and we are in good discussions which several parties but most important is that we can determine basically our own time-lines and our support by PD1 but at that stage we don't want to enter – partnership on AFM13 already..

Okay understood great.

And then on AFM11, I was wondering if you could provide some more details on the two studies that you are planning in ALL and non-Hodgkin’s – and how I guess how do product calls log in and where do you see differentiation from other programs?.

Yes. So, the original protocol let me start it out with – at five weekly doses in the first week continued by three weekly doses in weeks two to four. That trail was initiated as we said end of last year and has been ongoing.

What has changed if clearly a few matters first there is further product on the horizon that are entering clinical trials with a different target product profile mostly along the half life. That is something that we needed to take into consideration.

Data point number two what we saw is with a negative [indiscernible] that has a half life of just about 12 hours data reported indeed in a melanoma trail and there it was shown that the drug was efficacious with a weekly dosing. So, the half life of 12 hours was good enough for a weekly dosing to provide complete and positive responses.

Why we decided to amend the trial and not run two non-Hodgkin lymphoma trail is a very simple explanation, the feedback from this scientific advisory report asking quite clear that the new trail is considered a much better trail in their minds much better in convenience and for other reasons and if we want to have initiate that trail as a separate study we probably could have enrolled patients in, first patient in about nine months.

We took the opportunity now to consolidate basically these two studies and amend the non-Hodgkin lymphoma study thereby we can immediately start with a more convenient dosing in these patients. I do not want to comment with more details on what we are currently doing in such trails.

The reason is very simple, one is it's very competitive as there are maybe 4-5 very similar modalities in clinical development and we would like to keep details as much as we can to us for those reasons.

What also has been enabled by this change of strategy is that we are now initiating a trail in acute lymphoblastic leukemia, originally that trial or those data would have been generated as a chunk to the non-Hodgkin lymphoma trial so we are really enhancing that.

We have not yet said when we can start enrollment of that trial but planning is still at an early stage. But as soon as we have more details we will update you..

Okay, great..

Thank you so much..

We will now take our next question from Chris Marai from Oppenheimer. Please go ahead..

Hi guys this is actually Michelle Gilson on for Chris.

We have been wondering how do you think about the half way [indiscernible] and have you looked at modulating the half life with them by slowing the half rate on the entire side or modulating their operate on the target side?.

Yes, good question. So, regarding half life what we have been doing we have been measuring the half life of our drug in the Hodgkin study and there we have created data for AFM13 and it turned up out that the half life was about 20 hours almost a day.

However, when we treat the patients with a weekly doses [indiscernible] we were seeing efficacy in such patients. So that means that in Hodgkin lymphoma we have administered four weekly doses to the patients and then has assessed change in tumor mass and fat and in three out of 13 patients we were seeing a cautiously response.

Regarding your questions on affinities to the cell they may play an important role in terms of the pharmoco-dynamic activity of our drugs. As the half life is only free drug that we are measuring.

What we have until now not yet fully measured is the half life of the drug that indeed bound to the immune cell because of the high affinities that we are routinely having so one – we are assuming that our drug have a or can may have a much longer half life in the circulation because of their attachment to these immune cells.

As fact we do not yet have stated that but this is something that we are exploring..

Okay. And could you put to sub units into – to enhance that ability..

Yes, there is ways of how we can enhance the half life when you mean so there is obviously such means but at this time we have – we are already exploring the pharmaco-dynamic effect of our drug and once we understand that then we can determine if half life is really of some advantage.

And interest point to one important factor if we are looking at the [indiscernible] data which has a very short half life and enhance the drug needed to be administered by continuous infusion.

However, such a drug will also have side effects and one way of resolving the side effects we’re to stop the infusion so enhance the half life indeed became an advantage of the drug.

So without hang ups we need to see how that works out but having a much longer half life this may not necessarily be a huge advantage in the administration of our drugs..

Okay, thank you. And then finally, when we think about AFM11 for PGFR3, you have evidence that this penetrates the NS and how do you look at the opportunity to enhance PGFR3 targeting for [indiscernible] that have minimal impression of the target? Dr.

Florian Fischer So regarding CG19 and CNS side effects it's still not clear how these side effects are caused. There are several theories out there but none of this has been proven so we don't know what the real reason is for that. If it is really, CD19 binding somewhere in the CNS or something else. So we cannot speak to that.

On [indiscernible] we are analyzing -- chemistry binding to too much issues and we will present such data at the SITC conference in November however we have also presented the post that's already in earlier conferences where we controlled binding in addition to TBM tissues for example to head and neck tissues..

Okay. Thank you guys..

We will not take our next question from Chris Howerton from Jefferies, please go ahead..

Hi, thanks for taking the question.

And I think most of my questions already been asked but I just wanted to clarify for ASM21, you moved forward in NK-cell engaging approach and is this kind of setting a stage where how you are thinking about solid tumors in general and I guess that's it?.

Okay hi, Chris thanks a lot. Yes we are moving forward with the EGF receptive REM3, CG16, the molecule has been generated and we will present first data at the SITC conference.

Obviously, we also are performing currently some translation of studies in order to compare NK-cell engagement and T-cell engagement having said that until now it's unclear which is the better choice for treating solid tumors with these modalities, there has been limited success with the T-cell engagement pathway and Affimed is kind of the pioneer in the setting of NK-cell engagement.

There is obviously a good role for natural killer cells because what we can with our approach we can increase the lymphocyte population within the tumor and if that leads to activation we may just see a cascade of further activities being enhanced such as antitumor presentation and a potential involvement of cytotoxic T-cells.

If that's possible with mono-therapy or in combination with some other checkpoint inhibitors we need to see.

There has been some historic assessment of tumor tissues of patients on the infiltration by natural killer cells in a kind of natural way and in Colleen cancer there has been nice publication out there, only about 30% of patients indeed has natural killer cells.

And in half of them that had natural killer cells also cytotoxic T cells who are observed and it appeared that particular group had a somewhat better prognosis as compared to those that didn't have any infiltrated.

So there are some hints that the infiltration of natural killer cells can be quite beneficial for patients however as I said I think it's the pioneer, we are the only one to have that current engager platform available and that's why we are investigating and have been generating further data on that..

So, just to clarify your decision and move forward with NK cell engagement based upon strategic value there efficacy or data driven reason?.

Well, we have the efficacy data seen for our NK-cell platform already in Hodgkin lymphoma and have now the data that we have generated in collaboration with cancer university which are quite compelling.

And hence what we are now doing, we are using Hodgkin obviously also as a model set team where we have tumor lesions that need to be basically that are not in the circulation so they are in the tissue and it can be considered as a kind of a solid tumor so that tumor is really establishing the proof of principle in a broader setting.

So, here we have the mono-therapy where we already have initial data and now we are optimizing this trial in the phase two so we are establishing proof of concept and in parallel we are running the trial of AFM13 in combination with PD1 so those data that we believe will be critically important also determine the validity of occasional approach in the solid tumor setting.

And obviously, we now have to invest because once if the state are positive if we have quite some lead in the entire space and they quickly move into solid tumor settings as I have said before it may include head and neck, it may include colleen cancer, it may include lung cancer so it's extremely large indications that we could target.

And again, here the idea is that with NK-cell engage you can significantly increase the lymphocyte population within the tumor and you may need one or the other checkpoint in order to pull your release the efficacy of such immune cells.

So, we feel that we currently have available there is a good set of early data in our hand that definitely allows us to build a pipeline at that stage already..

Okay, great. Thanks for answering the question..

We will now take our next question from [indiscernible], please go ahead..

Hi, good morning. Thanks for taking my question. This is Rahul from Noble Life Partners. So, couple of questions here looking in your further data at ASCO with the checkpoint with pre-clinical that was really good.

So related to that talking about using checkpoint in the liquid tumors like Hodgkin’s lymphoma, so the question here is checkpoint inhibitor generally have not been used for liquid tumors so how should we understand that I mean are we looking at any – are you looking at the same patient population that's using for the other trial but other checkpoint inhibitors or you are looking for sort of bone marrow where there is lymph nodes where there is with the high PDL1 or PD1 population, how should we look at that?.

Currently we are only planned to study in Hodgkin lymphoma, there were two PD1s already investigated showing quite good efficacy in such patients.

One learning obviously has been that the efficacy at least takes treatment of three months much better six months so you see – in enhancement of efficacy the longer you treat, something that we’re also pursuing for AFM13. Now as we already have the evidence that both PD1s are efficacious in Hodgkin’s Lymphoma.

Plus, Hodgkin’s Lymphoma has a higher degree of PD-L1 expression, so this is very good setting. Now, you may wonder if we already have very good efficacy, why do we need to do a combination. Also overall response rates look very high; the number of complete responders is much lower. That’s been in the range of 15% to 20%.

So if that number can be propelled into the range of 40% to 50% we may not only have a therapy that is applicable for patients in the [indiscernible] setting that’s where we are currently setting, but we may also consider moving this combination then to the frontline.

Because with the high number of complete responses, this may be considered that we also may have a high number of cure rates..

That’s helpful, thank you. Well, the next question I have is to really trying to get a better gauge of your future approach in solid tumors. Now, clearly solid tumors are far more heterogeneous. You don’t have SPD19 or SPD30 that is the prominent and the only culprits, so to say.

I know you are using EGFR and so on, but the fact that NK Cells are not restricted by antigen, is it not possible to harness NK Cells generally and bring them in close proximity to multiple tumor antigens either with a vaccine or other approaches? Will that play out better?.

Yes, that’s a very good point. I mean this is how we might think and that is definitely something of an advantage of the Natural Killer Cells approach and this is one way how you can think that approach may be indeed be advantageous over, for example, a T cell approach.

But again, if it is a mono therapy or if it is a combination therapy, again, here we’re applying and combining two approaches. So, while the NK Cell approach is really increasing the Lymphocyte population in the tumor, with, for example, a checkpoint you can release the brakes. So that means that the tumor always develops defensive mechanisms.

So, first it avoids the attachment of the immune cell, in particular, the Natural Killer Cell. But even if there is an attachment, there is a strong modulation of the tumor over the immune cell. And, as I say, you might just meet like very often in cancer therapies you might need respective smart combinations.

We just feel that the combination of an NK Cell approach with checkpoint approach can fulfill such a requirement. Obviously, the NK Cell then has the advantage of being much more promiscuous, but it also can lead to the subsequent activities that I described before that's advantage in presentation we may have involvement of T cells.

But are you getting a much – you may get a response that's much broader.

So we know that that is all early days but through – in newer assessment that we’ve done at the Stanford university we have some evidence that we do not only drive NK-cells into the tumor but that we also have an uptake of such toxic T cells especially in a combination of AFM13 and PD1.

So, there is compelling data but we need to – this is what we are doing throughout 2016 we are generating first set of data in the setting of Hodgkin lymphoma and by the time once we have the data we have a pipeline that we can move into the clinic in solid tumors and we are hoping that we have two maybe three candidates by that time ready that could go into phase one studies..

Right and just for my understanding here, just like T cells I mean, NK cells are suppressed in the tumor in the solid tumor micro environment as well correct?.

I guess so, yes. From what we are learning is that there is definitely a strong immune suppression by tumors by other secreting factors of regulation of certain cells receptors..

Okay, thank you that's all I have..

[Operator Instructions] There are no further questions..

Okay. Thanks a lot for listening and talk to you soon. Bye, bye..

This concludes today's conference call. Thank you for your participation. Ladies and gentlemen you may now disconnect..