Anca Alexandru - Head-Communications Adi Hoess - CEO Florian Fischer - CFO.

Analysts:.

Good day, welcome to the Affimed Fourth Quarter and Year End 2017 Financial Results & Corporate Update Conference Call. Today's conference is being recorded. At this time, I would like to turn the conference over to Ms. Anca Alexandru. Please go ahead..

Thank you. I'd like to welcome you to our investor and analyst call and the results for the fourth quarter and year end 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 financials.

Also on the call is Wolfgang Fischer, Affimed's COO; who will be available for questions in the Q&A session. Before we start, please note that this call and the Q&A session may contain forward-looking statements, including statements regarding our future financial conditions, 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 altogether. Affimed is harnessing the power of innate and adaptive immunity in oncology. Our approach is to develop immune cell engagers that eliminate tumor cells by engaging and activating the extra killer T-cells.

Our clinical and preclinical pipeline is based specifically on molecules with tetravalent bispecific antibody. We are an industry leader in NK-cells bispecific antibody format, we are in engagement and our lead product candidate, AFM13 is to our knowledge the most advanced NKs in engaging chemical development.

We are particularly in unlocking the full potential of NK-cells in immuneoncology through suitable combination approaches. Here we are aiming on the one hand to generate a conservative immune response through combinations of synergistic mechanisms 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 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 we'll provide an update on all our clinical programs, as well as our preclinical programs to date.

Slide 4; we have an unincumbent clinical and preclinical pipeline of NK and T-cell engagers with our NK-cell engagers being developed in hematologic diseases and solid tumors. Based on our NK-cell platform, we have one clinical and two preclinical programs in development.

And based on our T-cell platform, we have one program in our own clinical development. A second T-cell engager program based on our platform called AMV564 is being clinically developed by Amphivena Therapeutics, a company of which we own about 18.5%, fully diluted.

Slide 5; our pipeline offers several very promising opportunity and comprises highly differentiated and versatile engagers to activate innate and adaptive immunity.

Early product candidate AFM13 has shown positive efficacy data as monotherapy in Hodgkin lymphoma, and also in CD30 positive lymphoma which we believe represents a novel opportunity with limited competition, for example in anaplastic large-cell lymphoma or peripheral T-cell lymphoma.

We've also reported encouraging efficacy for AFM13 in combination with the checkpoint inhibitors. I'll provide more detail on the clinical data for AFM13 later in this call. AFM26 is a B-specific BCMA and specific in NK-cells engager that we are developing in multiple myeloma.

In particular, we aim to leverage BCMA as a target in autologous stem cell plant individual patients. As such, we believe NK-cell engagers represent above differentiated opportunity. Our EGFR targeting NK-cell engager AFM24 has the potential to widen the therapeutic window and address the patient population resistant to standard-of-care.

We are developing AFM24 as a first-in-class NK-cell engager in solid tumors and believe that AFM24 also has the opportunity to improve efficacy of checkpoint inhibitors. Our T-cell engager, AFM11 comprise about differentiated approach for CD19 positive malignancy, and particular for the treatment of diffused large T-cell and multiple cell lymphoma.

We believe that AFM11 represents a great opportunity for us and that with a potential to pace the fast market approval. Slide 6; in 2017 and early 2018, we made key hires to strengthen our management team and we've expanded our U.S. presence.

Furthermore, in February 2018 we successfully completed an underwritten public offering on the NASDAQ global market.

We raised a total of approximately $24.5 million or €92.7 million in net proceeds and we expect the proceeds from the transaction together with the existing cash in our balance sheet to fund operations at least until the fourth quarter of 2019. As announced yesterday, we're particularly happy to have appointed Dr. Leila Alland as CMO.

Leila will join us officially next Monday, and we are extremely pleased to have her on our team. Leila is a seasoned immuneoncology expert with broad expertise in developing oncology products for solid and hematological malignancy including Opdivo, [indiscernible].

Prior to joining Affimed, Leila held leadership positions at ‎Tarveda Therapeutics, AstraZeneca, Bristol-Myers Squibb and Novartis. Leila will be based in our New York office along with Cassandra Choe-Juliak, VP, Clinical U.S. and Denise Mueller, who heads Affimed's Commercial Strategy & Business Development Department.

As you know from our third quarter 2017 update in September 2017, we made another significant addition to our management team with Dr.Wolfgang Fischer who joined Affimed as COO from the Novartis Group. There he mostly recently served as Global Head of Program and Project Management of the Sandoz pharmaceutical activation [ph].

Wolfgang has over 20 years of R&D experience with a focus on oncology, immunology and pharmacology. Slide 7; here you can see an overview of our executive team, which we have strengthened considerably over the last year.

We now have a high quality joint [indiscernible] combining deep pharma and biotech expertise, as well as program, planning and execution of human oncology clinical development and importantly, also commercial strategy and business development expertise.

Slide 8; over the course of 2017 and in early 2018, we've made significant headway in validating our NK-cell engager approach, in particular through encouraging data from studies with our lead candidate AFM13. AFM13 is a CD33/CD16A targeting tetravalent bispecific molecule which we're developing as both, mono and combination therapy.

At ASH [ph] in December 2017 and in a press release in February 2018 we presented data indicating that AFM13 is efficacious and well-tolerated as monotherapy and in combination with the anti-PD1 antibody [indiscernible] Keytruda.

These data of AFM2 trails our ongoing Phase 1b of AFM13 in combination with Merck's Keytruda and Hodgkin lymphoma in which we have completed recruitment and from our investigator sponsor translation of Phase 1b/2a study of AFM13 in patients suffering from relapse or refractory CD30 positive lymphoma, with cutaneous manifestations which is led by Columbia University.

I'll provide more detail on the results of these trials a bit later in the call. We're also investigating AFM13 and investigator sponsored Phase 2a monotherapy study in Hodgkin lymphoma which is being led by the German Hodgkin Study Group.

This studies augment through recruiting patients for relapse or refractory to both, pentoxima bedoctin [ph] and anti-PD1. Slide 9; in early 2017 we announced a collaboration with the University of Texas, MD Anderson Cancer Center to evaluate AFM13 in combination with MD Anderson's NK-cell product where the clinical research activities are progressed.

In addition, we are exploring additional options for NK-cell engagers and together with our collaborators at that German Cancer Research Center, we have recently published a paper in cancer immunology research showing that AFM13 sensitizes NK-cells throughout. This could potentially allow NK-cells to achieve deeper clinical response.

We continue to advance preclinical programs such as AFM26, APCMA/CP16A specific NK-cell engager, and AFM24 and EGFR/CD16A specific NK-cell engager through preclinical development. Regarding our T-cell engager programs, we're seeing great opportunity with our differentiated proprietary formats which are highly specific.

And unique PK/PD profiles and do not compare non-specific activation of T-cells in absence of target cells. While to-date, several competitor programs presented with low ORR or a stock our two Phase 1 dose escalation trials of AFM11 are progressing well.

Innate trial in NHL we have recently completed the third dose cards and we have just learned that the [indiscernible] has agreed to move their trial into the fourth dose cohort. Innate study in patient suffering from ALL, we're currently recruiting into the fifth dose cohort.

Further clinical validation could come from Amphivena's AMV564, a CD33/CD3 specific T-cell engager based on our platform. Here our Phase 1 study is ongoing and recruiting in AML, Amphivena is also planning to initiate study in the MDS and is exploring the potential to address minor derived suppressor cells in solid tumors.

Slide 10; we believe that our platform is truly differentiated from others. We're developing tetravalent bispecific molecules and the bivalent binding to two receptors on two different cells enables high affinity binding through increased avidity while maintaining high specificity.

We believe that this is very important in order to obtain favorable safety profile. Furthermore, our versatile platform allows for development of molecules with multi-specificity and tailored to specific indications and settings with unique PK and PT profile.

Further distinguishing our approach while most immune cell engaging approaches to-date focus on T-cell, our technology platform reliably generates both, T and NK-cell engagers allowing us to exploit both, adaptive and innate immune mechanism. Slide 11; our approach of high affinity CD16A targeting on NK-cell is unique in the industry.

To our knowledge CD16A is the only receptor triggering ADCC and does not require any additional co-stimulant array signals. Importantly, CD16A is constitutively expressed in about 95% of NK-cells. We've optimized CD16A binding to maximize NK-cell mediated killing within upto 1,000 or greater affinity to CD16A as compared to monoclonal antibodies.

In addition, binding to CD16A is largely unaffected by a competing IgG's and major hurdle for NK-cell activation by IgG based structures such as monoclonal antibodies. This is particularly important as in the ground state CD16A on innate immune cell is occupied by polyclonal plasma IgG.

This creates a significant threshold for IgG based therapeutic antibodies as there is a huge excess of plasma IgG versus therapeutic antibodies. However, not for Affimed's CD16A targeting antibody. The unique epitope recognized by our NK-cell engagers results in them being virtually unaffected by plasma IgG.

Furthermore, CD16A binding is independent of the 15 equivalent polymorphisms. And finally, our highly specific NK-cells do not bind to CD16A neutrophils avoiding a surpassing effect.

We believe that these features are highly important in targeting malignant cells which escape elimination by current therapeutics, for example, cells with low target expression. Slide 12 shows preclinical data demonstrating the superior potency and efficacy of our tetravalent bispecific form.

As compared to Fc-enhanced IgG or Native IgG molecules our molecules possess the high potency and efficacy invitro as shown on the left side. On the right side, you can see that our NK-cell engagers can kill tumor cells with very low target expression.

For NK-cell engagers we have demonstrated invitro killing of cells with CD30 expression as low as few thousand receptors and even a few hundred receptors per cell such as shown here for the BCMA bearing tumor cells. All of these features result in overall increased potency and efficacy of our NK-cell engagers.

Slide 13; as mentioned earlier, we are generating clinically proof-of-concept for our NK-cell engager approach by developing our lead candidate AFM13 as mono and combination therapy, and I'd like to show you now that we have observed clinical efficacy in both, the mono and combination therapeutic settings.

AFM13 has already demonstrated safety and clinical efficacy in heavily pre-treated Hodgkin lymphoma patients in the Phase 1 study with tumor shrinkage observed in 62% of patients which was 8 out of 13 patients, and partial responses in 23% of patients, which was 3 out 13.

None of the patients experiencing a PR had been previously treated with [indiscernible] or PB.

As previously communicated, dated from our investigator sponsored Phase 2a trial for AFM13 in relapse refractory Hodgkin lymphoma which is led by the German Hodgkin Study Group showed for the first time that AFM13 is efficacious as a single agent in heavily pre-treated group of patients and in particular that AFM13 is efficacious post PV.

Partial responses were observed in 2 out of 7 evaluable patients and growth under the study's original protocol who had been pretreated with PB but where [indiscernible]. And the data that's generated in the study including confirmation of the Safe Harbor safety program in our Phase 1 study represents important information on AFM13 combination study.

Slide 14; we announced in August 2017 that Columbia University had initiated a translational Phase 1b/2a study to evaluate AFM13 in patients with relapse or refractory CD30 positive lymphoma with cutaneous manifestations.

Recall that this trial is designed to allow for serial skin biopsy's thereby enabling assessment of NK-cell biology and tumor cell killing within the tumor environment. The first and the second cohorts have been fully enrolled and recruitment into the third cohort is ongoing.

CD30 positive lymphoma was cutaneous manifestation comprises of number of different sub-indications. In paper, we see represented data from the first 3 patients enrolled into our ISG who -- 2 were suffering from anaplastic large-cell lymphoma with cutaneous manifestations and 1 suffering from transformed mycosis fungoides or TMF in short.

All 3 patients were treated with AFM13 at 1.5 mg once weekly for 8 weeks and response data as determined by global response core showed one complete response, one partial response, both in the ALCL patient. These images here on the left show upper body skin lesions of the patients before and after treatment.

On the right hand side, the PET Scan results from the patients experiencing the complete response are detected and you can see the metabolic response at the area marked by the green arrows. These results are very encouraging as they provide further evidence that NK-cell engagers are able to induce tumor regression in this indication.

Off note, while the TMF patient experienced only stable disease, this is important to consider that this is a very severe form of the disease and that this patient had received 7 prior lines of treatment and never had a current stable disease before.

In general, the few CD30 positive lymphoma as an attractive indication that may broaden the potential for AFM13. Slide 15; tumor immune evasion impairs both NK-cell and T-cell functions, and therefore optimize approaches build in both innate and adaptive immunity.

NK-cell and T-cells are very different in how they recognize the tumor; while an NK-cell shows non-specific recognitions, T-cells are only active once they can specifically recognize a tumor; hence the mechanisms by which a tumor can prevent destruction are very different.

While for NK-cells, the ability to recognize tumor cells maybe a key mechanism, for T-cells it is the inhibition of their activation, for example, through checkpoint inhibitors.

In this context we have generated data in Hodgkin lymphoma both invitro, invivo and in patients combining treatments targeting innate and adaptive immunity, some of which are shown on the next slide. This slide shows the investigation of AFM13 in combination with Merck's Keytruda.

In the invivo PDX models we were able to show that AFM13 synergizes with anti-PD1 for tumor control and lymphocyte infiltration. In addition, AFM13 induces rapid NK cell infiltration as early as day 2 after treatment starts.

The synergy between AFM13 and an anti-PD1 antibody and PDX model provides a strong rational for the combination of AFM13 with checkpoint inhibitors and we are investigating this in an ongoing Phase 1b trial in relapse refractory Hodgkin lymphoma.

Here we have completed recruitment with a total of 30 patients recruited into the study 24 which are being treated at the highest AFM13 dose level vested during dose escalation.

In February 2018, we presented interim data from a total of 9 patients in this cohort demonstrating that AFM13 in combination with Keytruda is well tolerated with a 3-month of response rate of 89% comparing favorably to a historic ORR of 58% to 63% described for anti-PD1 monotherapy in a similar patient population of PV, pre-treated and un-treated PD1 naïve patients.

When looking specifically at trails of Keytruda's monotherapy with a more diverse patient population, our data also compares favorable; for example, the keynote of 13 study has achieved 65% overall response rate and in the keynote of 87 registration trial of 68% were reported.

Furthermore, in our study 4 out of 9 patients which are 44% showed complete metabolic responses versus 9% to 22% reported for anti-PD1 monotherapy and 16% to 22% reported specifically for Keytruda monotherapy studies. We expect full 3-months data by mid-year 2018 and to provide regular update at scientific and medical conference.

It is important to note that both overall responses and complete responses compare favorable to monotherapy data because for anti-PD1 monotherapy, not only CRs but also the partial responses have been described to be durable in this patient set.

Slide 17; additional opportunities for our NK-cell engagers in few combination with adoptive NK-cell transfer. Exvivo extension and stimulation of autologous NK-cells followed by reinfusion and combination with NK-cell engagers is a novel therapeutic concept.

In this combination, a large number of preactivated NK-cells can be redirected by our individual engagers to recognize malignant cells. This approach is independent of patients own NK-cell count and has potential applicability at the time of or shortly after autologous stem cell transplant.

We're investigating this approach with our partner MD Anderson. Initially we plan to investigate AFM13 with MDACC's NK cell product in the transplant set [ph]. 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 HL may pave way for combinations in further indications such as multiple myeloma. We hold an option to exclusive to ultimate drives to develop and commercialize any product developed under the collaboration.

Discovering and assessing additional opportunities to harness innate and adaptive immunity, I mentioned earlier, that we recently published data in Cancer Immunology Research. Together with our collaboration partner, the German Cancer Research Center, we presented evidence of AFM13 sensitizing NK-cells to [indiscernible] and/or stimulation.

After exposure to AFM13, the NK-cells showed enhanced IL2 and IL15 mediated proliferation and cytotoxicity. These data collaborate initial findings represented at ANCR last year and support the approach of combining NK-cell engagers with IL2 or IL15 to potentially achieve clinical responses.

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 two most transplant [ph] candidates AFM24 and AFM26.

Slide 18; we are developing AFM26 and NK-cell engaging by specific antibody targeting T-cell maturation antigen to address the medical need for a novel approach to treat multiple myeloma.

In particular, we aim to leverage BCMA as a target in autologous stem cell transplant in patients with treatment at or shortly after ASCT offering the potential to eliminate minimal residual CDs, GCs avoiding relapse.

We believe BCMA is a highly promising target for therapeutic intervention based on early clinical data, by the low expression of BCMAs as a significant hurdle to eliminate malignant cells. NKs are the first population of lymphocytes to recover post-transplant; thus offering the opportunity to exploit AFM26 and the parent transplant cell.

Preclinical development of AFM26 is ongoing, we're developing different tetravalent and bispecific antibody performance and how selective the final can be [ph].

AFM26 employs a unique mechanism of action through high affinity engagement of NK cell, invitro efficacy against doubt expressed in very low levels of BCMA and NK-cell binding largely by IgG computation.

In addition, AFM26 offers the opportunity for combination with adoptive NK-cell transfer as it appears to have a favorable safety profile with lower cytokines as compared to BiTE.

Slide 19; despite several marketed agents such as cetuximab and other tyrokinase inhibitors, there is a significant medical need for a novel approach to treat EGFR positive tumors. This requires widening the therapeutic window and addressing treatments. Existing targeted therapies function through blocking the signaling activity of EGF receptor.

Our approach is different because we're pursuing EGF as a target to increase immune cell killing at the site of the tumor. Our goal is to address the limitations of existing drugs by improving both, efficacy and safety.

In particular, there is no clear indication of efficacy of EGFR blocking antibodies in patients with Ras mutations and severe skin toxicity may impact a physicians willingness to prescribe a drug. Affimed has generated 2 candidates called AFM24-T, AFM24-I.

These two EGFR/CD16A targeting molecules possess different PKs and PDs but offer differentiated mode of action functioning through NK-cell killing. They show increased potency compared to cetuximab, enabling NK-cell mediated killing of cells expressing low levels of EGFR.

Our goal is to address a broad patient population including patients resistant to EGFR targeting agents. Pilot TOX studies in [indiscernible] with AFM24 have been encouraging and showed first evidence of a beneficial profile when administered as single a repeated dose.

AFM24 TOX studies are planned for 2018 and the company anticipates completing Ig enabling studies by mid-year 2019. Slide 20; our approach is much differentiated from existing approaches as we have selected an antibody recognizing EGF receptor with high affinity but with reduced no blocking of EGF-induced signal transduction.

This could lead to an improved safety profile. We engineered an NK-cell engager to achieve high potency and efficacy, and Slide 20 shows that AFM24 can induce complete tumor growth control in an invivo model. Slide 21; now jumping to our T-cell based approaches.

For T-cell based immunotherapies, CAR-Ts have recently taken the lead however bispecific antibody based platforms can address certain week.

T-cell based anti-tumor therapies have been clinically validated for CD19 and BCMA but are limited by significant associated toxicities including CRS and neurotoxicity, as well as high COGS and limited accessibility, especially for CAR-Ts.

As for immune selling data, different platforms are in development with short-lived molecules such as BiTEs and DARTs reporting evidence of good efficacy while long-lived platforms have faced that including low -- overall response rate and even stopped trials.

As mentioned earlier, our tetravalent bispecific antibody platform has several differentiating features and two programs are in clinical development with the potential for fast development timeline, AFM11 developed by Affimed and AMV564 developed by Amphivena.

Slide 22; we believe that our platform has the potential to overcome the challenge to find the optimal therapeutic window with a T-cell engage. No non-specific activation of T-cells is observed in absence of target cells and we were able to target tumor cells with very low target expression.

The lysis of tumor cells appears to be independent of a number of T-cells. We also offer a significant improved PK versus the BiTE. Our lead T-cell engager product candidate AFM11 is in clinical development and we are in the process of determining the recommended Phase 2 dose.

Two Phase 1 dose escalation studies trials are ongoing in patients with relapse refractory ALL and with relapse refractory NHL respectively. In NHL we have recently completed the third dose cohort and we have just learned that the review committee -- Phase 2 review committee has agreed to move the trial into the fourth dose cohort.

In ALL, we're currently recruiting into the fifth dose cohort. Important to note is that based on our preclinical data, we believe that the active dose might be somewhere in the range of dose levels 5 to 7.

With our T-cell engagers, we have the potential to pave the path to fast market approval in indication such as diffused [indiscernible] or multiple cell lymphoma. As mentioned earlier, Amphivena is clinically developing AMV564, a CD33/CD3 specific antibody based on our platform.

Amphivena continues to recruit patients into it's first human Phase 1 dose escalation study of AMV564 in relapse refractory AML. Amphivena also plans to launch a Phase 1 clinical study in patients with MDS, and is exploring the utility of AMV564 in solid tumors.

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. Any numbers referring to the Q4 2017 and Q4 2016 are unaudited whereas annual numbers for 2017 and 2016 are audited.

Cash and cash equivalents and financial assets totaled €39.8 million as of December 31, 2017, compared to €44.9 million as of December 31, 2016. Affimed's was able to fund it's operational expenses in 2017 with existing cash, the issuance of new shares and the usage of additional loan trench.

Taking the consummation of our public offering in February 2018 into consideration, cash and cash equivalents would have been on a pro forma basis, €64.2 million as of December 31, 2017. Net cash used in operating activities for the fourth quarter of 2017 was €4.9 million compared to €6.6 million for the fourth quarter of 2016.

Net cash used in operating activities was €25.5 million for the 12 months ended December 31, 2017 compared to €32.1 million for the 12 months ended December 31, 2016. The year-to-year decrease was primarily related to lower cash expenditure for research and development in connection with our development and collaboration programs.

Including the proceeds from the offering in February 2018, Affimed expects to have cash to fund our operations at least until the fourth quarter of 2019. This provides runway for the planned development of our clinical programs, as well as for further discovery and early development activity.

Revenue for the fourth quarter 2017 was €0.6 million compared to €1.4 million for the fourth quarter in 2016. Revenue for the full year 2017 was €2.0 million compared to €6.3 million for the full year 2016. Revenue for the full year and the fourth quarter 2017 was primarily derived from AbCheck Services.

Revenue for the full year 2016 related to Affimed's collaboration with Amphivena, the LLS, and AbCheck Services; while revenue for the fourth quarter 2016 was derived only from AbCheck Services. R&D expenses for the fourth quarter 2017 were €4.6 million compared to €5.7 million for the fourth quarter in 2016.

For the full year 2017, R&D expenses were €21.5 million compared to €30.2 million for the full year 2016. The decrease was primarily related to lower expenses for AFM13 related to CMC activities, preclinical programs and infrastructure.

G&A expenses for the fourth quarter in 2017 were €1.9 million compared to €2.1 million for the fourth quarter in 2016. For the full year 2017 G&A expenses were slightly lower, with €8.0 million compared to €8.3 million for the full year 2016.

Net loss for the fourth quarter 2017 was €6.4 million or €0.14 cent per common share compared to a net loss of €5.4 million or €0.19 per common share for the fourth quarter of 2016. Net loss for the full year 2017 was €30.2 million, or €0.69 per common share compared to a net loss of €32.2 million or €0.97 per common share for the full year 2016.

The decrease in net loss for the full year 2017 was primarily related to decreased spending on R&D for AFM13 related CMC activities, preclinical programs and infrastructure, partially offset by lower revenue and higher finance costs.

Additional information regarding these results is included in the north to the consolidated financial statements as of December 31, 2017 and Item V, operating and financial review and prospects which are included in Affimed's Annual Report on Form 20-F as filed with the SEC.

I will now turn the call back over to Adi for a summary of our two clinical programs and our pipeline.

Adi?.

Thanks, Florian. As already mentioned, our strategy is to maximize the value in our incumbent clinical and pre-clinical pipeline of NK and T-cell engagers as well as from our platform. As described by leveraging our lead product AFM13 as monotherapy in CD30 positive lymphoma and in combination with Keytruda in Hodgkin lymphoma.

Focusing on salvage settings for example, on relapse refractory ALCL or P2CO [ph] could enable a fast development path and allowing the establishment of a cost efficient marketing Intel's infrastructure. In addition, we believe investigating AFM13, both as monotherapy and in combination with Keytruda reduces it's development risk.

Another focus of your activities is the exploration of NK-cell engagers in combinations with checkpoint, modulators, adoptive NK-cells or immune-activating agents such as IL2 and IL15. In hematological diseases, we intend to leverage additional opportunities for AFM13 and AFM26 in such combinations.

Overall, our preclinical and clinical strategy is designed to broaden the scientific leadership of our NK-cell platform. Consequently, we are expanding the preclinical and clinical activities of our tetravalent bispecific NK-cell engager platform in solid tumors with our preclinical candidate AFM24.

We're also developing T-cell engagers and our lead T-cell engager AFM11 is being investigated in two ongoing ALL and NHL trials. AMV564, a T-cell program derived from our platform is in clinical development through Amphivena to treat AML.

In addition, as mentioned earlier, moving beyond our tandem [ph] format, we're developing different tetravalent bispecific antibody formats, tailored to specific indications inside [ph]. Thanks a lot for your interest. The call is now open for questions..

Operator:.

Thanks a lot. If there are no questions at this time, then I'll thank you for listening to our earnings call year-end and fourth quarter. And if there are any follow-up questions, please don't hesitate to reach out to us, and I wish you all a nice day. Thanks a lot again..

Thank you, ladies and gentlemen, that concludes today's call. You may now disconnect..