Affimed NV (AFMD) 2017 Q4 法說會逐字稿

Good day, and welcome to the Affimed Fourth Quarter and Year-end 2017 Financial Results and Corporate Update Conference Call. Today's conference is being recorded.

At this time, I would like to turn the call over to Ms. Anca Alexandru. Please go ahead.

Thank you. I'd like to welcome you to our investor and analyst call 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 CFO, who will be available for questions in the Q&A session.

Before we start, please note that this call and the Q&A session contain forward-looking statements, including statements regarding our future financial condition, business strategy and our plans and objectives for future operations. These statements represent our beliefs and assumptions only as of the date of this discussion.

Except as required by law, we assume no obligation to update these forward-looking statements publicly or to update the reasons why actual results could differ materially from those anticipated in the forward-looking statements, even if new information becomes available in the future.

These forward-looking statements are subject to risks and uncertainties, and actual results may differ materially from those expressed or implied in the forward-looking statements due to various factors, including, but not limited to, those identified under the section entitled Risk Factors in our filings with the SEC, and those identified under the section entitled Cautionary Statements Regarding Forward-Looking Statements in our Form 6-K filed with the SEC today. Thank you for your understanding.

I will now hand the call over to our CEO, Adi Hoess, who will provide a corporate update.

Thank you, Anca, and good morning all together. 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 natural killer or T cells. Our clinical and preclinical pipeline is based specifically on molecules with a tetravalent bispecific antibody.

We are an industry leader in NK cell bispecific antibody format. We are in engagement and our lead product candidate, AFM13, is, to our knowledge, the most advanced NK cell engager in clinical development. We are particularly interested in unlocking the full potential of NK cells in immuno-oncology through suitable combination approaches. Here we are aiming, on the one hand, to generate a concerted immune response through combinations of synergistic mechanism, for instance by combining our product with checkpoint inhibitors or cytokines, such as IL-2 or IL-15. 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 T cell-based approach, which includes our own clinical candidate, AFM11, and we'll provide an update on all our clinical programs as well as our preclinical programs today.

Slide 4. We have an unencumbered 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 1 clinical and 2 preclinical programs in development. And based on our T cell platform, we have 1 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 opportunities and comprises highly differentiated and versatile engagers to activate innate and adaptive immunity. Our lead 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 inhibitor, Keytruda. I'll provide more detail on the clinical data for AFM13 later in this call.

AFM26 is a B-specific -- BCMA specific NK cell engager that we are developing in multiple myeloma. In particular, we aim to leverage BCMA as a target in autologous stem cell transplant-eligible patients and effecting why we believe NK cell engagers represent more 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're developing AFM24 as a first-in-class NK cell engager in solid tumor and believe that AFM24 also has the opportunity to improve efficacy of checkpoint inhibitors.

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

Slide 6. In 2017 and early 218 (sic) [2018], we made key hires to strengthen our management team and we've expanded our U.S. presence. Furthermore, in February 218 (sic) 2018 , we successfully completed an underwritten public offering on the NASDAQ Global Market. We raised a total of approximately USD 24.5 million or EUR 19.7 million in net proceeds, and we expect the proceeds from the transaction together with the existing cash and 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 immuno-oncology expert with broad expertise in developing oncology products for solid and hematological malignancies, including Opdivo, Tagrisso and Tasigna. 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 and 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, where he most recently served as Global Head of Program and Project Management of the Sandoz Biopharmaceuticals division. Wolfgang has over 20 years of R&D experience with a focus in 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 U.S. and U.S. team combining deep pharma and biotech expertise as well as program planning and execution of immuno-oncology, clinical development and importantly also commercial strategy and business development expertise.

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 CD30/CD16A-targeting tetravalent bispecific molecule, which we're developing as both mono and combination therapy. At ASH 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-PD-1 antibody, pembrolizumab or Keytruda. These data were from 2 trials: Our ongoing Phase Ib of AFM13 in combination with Merck's Keytruda in Hodgkin lymphoma, in which we've completed recruitment; and from our investigator-sponsored translation of Phase Ib/IIa study of AFM13 in patients suffering from relapsed 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 in an investigator-sponsored Phase IIa monotherapy study in Hodgkin lymphoma, which is being led by the German Hodgkin Study Group. This study is open and recruiting patients relapsed or refractory to both brentuximab vedotin and anti-PD-1.

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, a preclinical research activity in progress. In addition, we are exploring additional options for our NK cell engagers. And together with our collaborators at German Cancer Research Center, we have recently published a paper in Cancer Immunology Research showing that AFM13 sensitizes NK cells to IL-2- or IL-15. This could potentially allow NK cells to achieve deeper clinical response.

We continue to advance preclinical programs, such as AFM26, a BCMA/CD16A-specific NK cell engager, and AFM24, an EGFR/CD16A-specific NK cell engager through preclinical development.

Regarding our T-cell-engager programs, we see a great opportunity with our differentiated proprietary formats, which are highly specific. They have unique PK/PD profiles and do not confer nonspecific activation of T cells in absence of target cells. While to date, several competitor programs presented with low ORR or a stop, our two Phase I dose-escalation trials of AFM11 are progressing well. In a trial in NHL, we have recently completed the third dose cohort, and we have just learned that the review committee has agreed to move the trial into the fourth dose cohort. In a study in patients suffering from ALL, we're currently recruiting into the fifth dose cohort. Further clinically validation could come from Amphivena’s AMV564, a CD33/CD3-specific T cell engager based on our TandAb platform. Here a Phase I study is ongoing and recruiting in AML. Amphivena is also planning to initiate a study in the MDS and is exploring the potential to address myeloid-derived suppressor cells in solid tumor.

Slide 10. We believe that our platform is truly differentiated from others. We're developing tetravalent bispecific molecules and the bivalent binding to 2 receptors on 2 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 multispecificity and tailored to specific indications and settings with unique PK and PD profile.

Further distinguishing our approach, while most immune cell engaging approaches today 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 costimulatory signal. Importantly, CD16A is constitutively expressed in above 95% of NK cells. We've optimized CD16A binding to maximize NK cell-mediated killing with an up to 1,000 or greater affinity to CD16A as compared to monoclonal antibodies. In addition, binding to CD16A is largely unaffected by competing IgGs, a major hurdle for NK cell activation by IgG-based structures, such as monoclonal antibodies. This is particularly important as in the ground stage, CD16A on innate immune cells is occupied by polyclonal plasma IgG. This creates a significant threshold for IgG-based therapeutic antibodies as there is a huge excess of plasma IgG versus therapeutic antibody; however, not for Affimed's CD16A targeting antibody. The unique epitope recognized by our NK cell engagers result in them being virtually unaffected by plasma IgG. Furthermore, CD16A binding is independent of the 158 valent (inaudible) polymorphism. And finally, our highly specific NK candidate do not bind to CD16B on neutral folds, avoiding a double sync 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 format. As compared to Fc-enhanced IgG or native IgG molecules, our molecules possess a high potency and efficacy in vitro as shown on the left side. On the right side, you can see that our NK cell engagers kept -- killed tumor cells with very low target expression. For NK cell engagers, we've demonstrated in vitro killing of cells with CD30 expression as low as a 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 clinical 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 setting. AFM13 has already demonstrated safety and clinical efficacy in heavily pretreated Hodgkin lymphoma patients in the Phase I 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 of 13. None of the patients experiencing a PR have been previously treated with brentuximab vedotin or BV. As previously communicated, data from our investigator-sponsored Phase IIa trial for AFM13 in relapsed/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 pretreated group of patients, and in particular that AFM13 is efficacious post BV. Partial responses were observed in 2 out of 7 evaluable patients enrolled under the study's original protocol, who had been pretreated with BV, but were anti-PD1 naive. The dataset generated in this study, including confirmation of the favorable safety profile seen in our Phase I study, represents important information on -- for AFM13 combination study.

Slide 14. We announced in August 2017 that Columbia University had initiated a translational Phase Ib/IIa study to evaluate AFM13 in patients with relapsed or refractory CD30-positive lymphoma with cutaneous manifestation. Recall that this trial is designed to allow for serial skin biopsies, 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 with cutaneous manifestation comprises a number of different subindications. In February of this year, we presented data from the first 3 patients enrolled into our IST who -- 2 were suffering from anaplastic large-cell lymphoma with cutaneous manifestation and 1 suffering from transformed mycosis fungoides or TMS in short.

All 3 patients were treated with AFM13 at 1.5 mg per kg once weekly for 8 weeks. And response data as determined by global response core showed 1 complete response, 1 partial response both in the ALCL patients. 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 patient 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. Of note, while the TMF patients experienced only stable disease, it 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 his current state of disease before.

In general, we view 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 function, and therefore optimal I/O approaches build on both innate and adaptive immunity. NK cell and T cells are very different in how they recognize the tumor, while an NK cell shows nonspecific recognition, T cells are only active once they can specifically recognize a tumor. Hence the mechanisms by which a tumor can prevent destruction are very different. While for NK cells, the ability to recognize tumor cells may be 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 in vitro, in vivo and in patients combining treatments targeting innate and adaptive immunities, some of which are shown on the next slide.

This slide shows the investigation of AFM13 in combination with the Merck's Keytruda. In, in vivo 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 in PDX model provides a strong rationale for the combination of AFM13 with the checkpoint inhibitors, and we are investigating this in an ongoing Phase Ib trial in relapsed/refractory Hodgkin lymphoma.

Here we have completed recruitment with a total of 30 patients recruited into the study, 24 of which are being treated at the highest AFM13 dose level tested 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 objective response rate of 89% comparing favorably to an historic ORR of 58% to 63% described for anti-PD1 monotherapy in a similar patient population of BV pretreated and anti-PD1 naive patients.

When looking specifically at trials of Keytruda's monotherapy with a more diverse patient population, our data also compares favorably. For example, the KEYNOTE-013 study has achieved 65% overall response rate, and in the KEYNOTE-087 registration, trials of 68 were reported -- 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 study.

We expect full 3 months data by midyear 2018 and intend to provide regular update at scientific and medical conferences. It is important to note that those 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 setting.

Slide 17. Additional opportunities for our NK cell engagers include combinations with adaptive NK cell transfer. Ex vivo expansion and stimulation of autologous NK cells followed by reinfusion in combination with NK cell engager is a novel therapeutic concept. In this combination, a large number of preactivated NK cells can be redirected by our NK cell 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 setting. Preclinical research activities are on track and these are intended to followed by a Phase I 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 development rights 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 have recently -- 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 IL-2 and/or IL-15 stimulation. After exposure to AFM13, the NK cells showed enhanced IL-2 and IL-15-mediated proliferation and cytotoxicity. These data corroborate initial findings we presented at AACR last year and support the approach of combining our NK cell engagers with IL-2 or IL-15 to potentially achieve deeper clinical response.

In addition to our clinical programs, we have an innovative preclinical pipeline addressing both hematologic indications and solid tumor. Over the last quarter we have further characterized our 2 most advanced preclinical candidates, AFM24 and AFM26.

Slide 18. We're developing AFM26, an NK cell engaging bispecific antibody targeting B-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-eligible patient with treatment at or shortly after ASCT offering the potential to eliminate minimal residual disease avoiding relapse.

We believe BCMA is a highly promising target for therapeutic intervention based on early clinical data, but low expression of BCMA is a significant hurdle to eliminate malignant cells. NK cells are the first population of lymphocytes to recover post transplant, thus offering the opportunity to exploit AFM26 in the peri-transplant phase. Preclinical development on -- of AFM26 is ongoing. We are developing different tetravalent bispecific antibody formats and have selected the final candidate. AFM26 employs a unique mechanism of action through high affinity engagement of NK cells, in vitro efficacy against cells expressing very low levels of BCMA and NK-cell binding largely unaffected by IGT competition. In addition, AFM26 offers the opportunity for combination with adoptive NK cell transfer as it appears to have a favorable safety profile with lower cytokine release as compared to a BiTE.

Slide 19. Despite several marketed agents such as cetuximab and other tyrosine kinase inhibitors, there is a significant medical need for a novel approach to treat EGFR positive tumors. This requires widening of the therapeutic window and addressing treatment. 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 mutation, and severe skin toxicity may impact a physician's willingness to prescribe a drug.

Affimed has generated 2 candidates called AFM24-T, AFM24-I. These 2 EGFR/CD16A targeting molecules possess different PKs and PDs, but both offer a 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 agent. Pilot tox studies in cynomolgous monkeys with AFM24 have been encouraging and showed first evidence of a beneficial profile when administered as single and repeated dose.

AFM24-I tox studies are planned for 2018 and the company anticipates completing IND enabling studies by midyear 2019.

Slide 20. Our approach is much different -- 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 designed to achieve high potency and efficacy, and Slide 20 shows that AFM24 can induce complete tumor growth control in an in vivo model.

Slide 21. Now jumping to our T cell-based approaches. With T cell-based immunotherapies, CAR-Ts have recently taken the lead. However, bispecific antibody-based platforms can address certain weaknesses. T cell-based antitumor 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 cell engagers, 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 setbacks, including low overall response rates 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 time lines, AFM11 developed by Affimed and AFM564 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 engager. No nonspecific 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 to the 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 II dose. Two Phase I dose-escalation studies -- trials are ongoing in patients with relapsed/refractory ALL and with relapsed/refractory NHL, respectively. In NHL, we have recently completed the third dose cohort, and we have just learned that the review committee -- safety 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 indications, such as diffuse large-B or mantle cell lymphoma.

As mentioned earlier, Amphivena is clinically developing AMV564, a CD33/CD3-specific antibody based on our TandAb platform. Amphivena continues to recruit patients into its first-in-human Phase I dose-escalation study of AMV564 in relapsed/refractory AML. Amphivena also plans to launch a Phase I 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 Q4 2017 and Q4 2016 are unaudited, whereas annual numbers for 2017 and 2016 are audited.

Cash and cash equivalents and financial assets totaled EUR 39.8 million as of December 31, 2017, compared to EUR 44.9 million as of December 31, 2016. Affimed was able to fund its operational expenses in 2017 with existing cash, the issuance of new shares and the usage of additional loan tranche. Taking the consummation of our public offering in February 2018 into consideration, cash and cash equivalents would have been on a pro forma basis EUR 64.2 million as of December 31, 2017.

Net cash used in operating activities for the fourth quarter of 2017 was EUR 4.4 -- EUR 4.9 million compared to EUR 6.6 million for the fourth quarter of 2016. Net cash used in operating activities was EUR 25.5 million for the 12 months ended December 31, 2017, compared to EUR 32.1 million for the 12 months ended December 31, 2016. The year-over-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 2019. This provides runway for the planned development of our clinical programs as well as for the further development and discovery and early development activities.

Revenue for the fourth quarter 2017 was EUR 0.6 million compared to EUR 1.4 million for the fourth quarter in 2016. Revenue for the full year 2017 was EUR 2.0 million compared to EUR 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 EUR 4.6 million compared to EUR 5.7 million for the fourth quarter in 2016. For the full year 2017, R&D expenses were EUR 21.5 million compared to EUR 30.2 million for the full year, 2016. The decrease was primarily related to lower expenses for AFM13-related CMC activities, preclinical programs and infrastructure.

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

Net loss for the fourth quarter 2017 was EUR 6.4 million or EUR 0.14 per common share compared to a net loss of EUR 5.4 million or EUR 0.19 per common share for the fourth quarter in -- of 2016. Net loss for the full year 2017 was EUR 30.2 million or EUR 0.69 per common share compared to a net loss of EUR 32.2 million or EUR 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 notes to the consolidated financial statements as of December 31, 2017, and Item 5, 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 2 clinical programs and our pipeline. Adi?

Thanks, Florian. As already mentioned, our strategy is to maximize the value in our unencumbered clinical and preclinical pipeline of NK and T cell engagers as well as from our platform. As described, we're 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 relapsed/refractory ALCL or PTCL could enable a fast development path and allowing the establishment of a cost-efficient marketing and sales infrastructure. In addition, we believe investigating AFM13 both as monotherapy and in combination with Keytruda reduces its development risk. Another focus of our activities is the exploration of NK cell engagers in combinations with checkpoint modulators, adoptive NK cells or immune activating agents such as IL-2 or IL-15. In hematologic 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 platforms in solid tumors with our preclinical candidate, AFM24.

We are also developing T cell engagers and our lead T cell engager, AFM11, is being investigated in 2 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 TandAb format, we are developing different tetravalent bispecific antibody formats tailored to specific indications and sets. Thanks a lot for your interest. The call is now open for questions.

(Operator Instructions) There are currently no questions in the queue at this time. (Operator Instructions) Again, there are currently no questions at this time.

Yes. thanks a lot. If there are no questions at this time, then I will 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.