Affimed N.V. (NASDAQ: AFMD) Q1 2020 Earnings Call Transcript

Affimed N.V. (AFMD) Q1 2020 earnings call dated Jun. 23, 2020

Corporate Participants:

Alexander Fudukidis — Head of Investor Relations

Adi Hoess — Chief Executive Officer

Arndt Schottelius — Chief Scientific Officer

Andreas Harstrick — Chief Medical Officer

Michael Wolf — Head of Finance

Wolfgang Fischer — Chief Operating Officer

Analysts:

Maury Raycroft — Jefferies — Analyst

Jim Birchenough — Wells Fargo — Analyst

Yale Jen — Laidlaw & Company — Analyst

Ike Oji — BMO Capital — Analyst

Presentation:

Operator

Good day and welcome to Affimed’s First Quarter 2020 Financial Results and Corporate Update Conference Call. At this time, all participants are in a listen-only mode. As a reminder, today’s conference is being recorded. I will now introduce your host for today’s conference, Alexander Fudukidis, Head of Investor Relations at Affimed. Please go ahead.

Alexander Fudukidis — Head of Investor Relations

Thank you, Bernard. I would like to welcome and thank you all for joining us today for Affimed’s first quarter 2020 financial results and operational progress. This morning, Affimed issued a press release, which is also posted on our website at www.affimed.com. On the call today, we have with us Doctors Adi Hoess, our Chief Executive Officer; Andreas Harstrick, our Chief Medical Officer; and Arndt Schottelius, Chief Medical [Phonetic] Officer; and Michael Wolf, Head of Finance. We are also joined by Dr. Wolfgang Fischer, Chief Operating Officer; and Ms. Denise Mueller, Chief Business Officer. They will all be available for the Q&A session.

We will begin today’s call with opening remarks from Adi on the Company’s operational update. Arndt will give you a brief background about our design [Phonetic] and the AACR process presented yesterday. And Andreas will provide an update on our clinical programs. Finally, Michael will review the financial results for the first quarter. After the prepared remarks, we will open the call for a Q&A session.

Before we start, I will review our Safe Harbor statement. Today’s discussion contains projections and forward-looking statements regarding future events. These statements represent our beliefs and assumptions only as of the date of this call. 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 under the section entitled Forward-Looking Statements in the press release that we issued today and filed with the SEC.

With that, I will turn the call over to Adi. Adi?

Adi Hoess — Chief Executive Officer

Thank you, Alex, and good morning, everyone. Thank you for joining us for this update call. We have a few operational updates that we’re going to share along this conference call. But first, let me say that I hope that you and your families are well and safe. We know that COVID continues to affect our societies all around the world, now facing the new challenge of learning how to best reopen our countries and the businesses. We’re beginning to do so carefully in Europe, and we are hoping that the situation will turn around in US in the near future as well.

Today, we will use a slide presentation, and I will guide you through which slide I’m speaking to, and I will start on Slide 3 of our presentation. At Affimed, our vision is to stop cancer from derailing the lives of patients by providing novel therapies that take advantage of the potential of the innate immune system. We are at the forefront of developing innate cell engagers based on our ROCK platform with the aim of addressing patients that currently have limited treatment options.

We believe that this represents a large opportunity as this could improve efficacy, tolerability and has the potential to treat previous non-responders to standard of care. On this end, we are quite honored to work with the world’s leading academic institutes and industry pioneers of oncology drug development, who pursue innate cell engager product development in a large number of oncology indications [Phonetic]. All this work has transformed Affimed from an engineering company into a late stage product company, with AFM13 being developed in a registration directed study in peripheral T-cell lymphoma, and we are pursuing an innovative approach, which is the combination of AFM13 with [Indecipherable] NK cell therapy. This indeed may be applicable to any of our innate cell engagers [Technical Issues]. We have further built a broad pipeline comprising products in different phases of development, [Indecipherable] and solid tumor indications.

As presented on our posters at this second virtual AACR, our ROCK platform can generate a diverse set of innate cell engagers with promising preclinical activity and good safety profile. The basis for all our programs is the industry-leading ROCK platform, which develops — which enables us to develop fully owned products and partner programs. These efforts are led by a seasoned team of experts at Affimed, and we’re well funded. As we announced in our earnings calls, we have a good cash position that allows us to pursue several programs that could deliver multiple value [Phonetic] inflection points.

I’m now turning to Slide 5 to give you an update on our management. So, since the beginning of 2020, we have strengthened our management team with the addition of key industry leaders who are on the call with me: Dr. Andreas Harstrick, who is our new Chief Medical Officer; and Arndt Schottelius, who is our Chief Scientific Officer. Earlier this month, we also announced the addition of Angus Smith, who will come onboard in July as the Company’s Chief Financial Officer. Angus joins us from Rockwell Medical where he held the role of Chief Financial Officer and brings with him best capital markets and biopharmaceutical industry experience. All these additions bring expertise, industry know-how and fresh ideas to Affimed. I’m indeed looking forward to working with this high-caliber management team to ensure the execution of our company’s strategy and achieve our goal of delivering new medicines that give patients back the innate ability to fight cancer.

For those of you who follow our story, you know that we currently have two innate cell engagers in clinical development, AFM13 and AFM24, and two in preclinical development, AFM28 and AFM32. We also have work ongoing on multiple candidates as part of the Genentech collaboration.

I’m now turning to Page 6 that gives you the overview of our pipeline. We will provide an update on the programs, along with preclinical highlights from our presentation at yesterday’s AACR meeting on AFM24. Our researchers presented on this bispecific EGFR/CD16A innate cell engager that has the potential to overcome multiple challenges that exist with current treatments for EGFR-positive malignancies that have resistance [Phonetic] and a challenge to safety profile of existing therapies.

Our research also featured — was also featured on a second poster that was presented by Genentech on the preclinical pharmacology and safety of RO7297089, previously known as AFM26, a novel bispecific BCMA/CD16A innate cell engager for the treatment of multiple myeloma. Both posters showed potent killing in tumor cell lines with low target expression in preclinical model, and our Chief Scientific Officer, Arndt Schottelius, will share some of the key highlights. Following Arndt, Andreas will provide an update on the progress we are making with the clinical development program, including details around the recent news we shared last week on AFM24, gearing [Phonetic] the first dose cohort in the Phase I/IIa study of AFM24.

Let me quickly give you an update on our financial situation, position — our cash position indeed being [Phonetic] EUR88.2 million. In addition, since May 13, the Company raised net proceeds of EUR18.8 million under its at-the-market, ATM, program. The pro forma cash position of the Company as of March 31, 2020, including the net proceeds from the ATM, has been EUR107 million. The cash infusion is planned to be used to support the broader development strategy of — for AFM24. As communicated in our year-end earnings call, we expect our cash position is sufficient to build on our momentum and fund operations well into the first half of 2022.

The final update will be from Michael, who will review the first quarter financials. I will now turn the call over to Arndt.

Arndt Schottelius — Chief Scientific Officer

Adi, thank you. And before we start, I’d like to briefly introduce myself to those who are new to the Company and Affimed and tell you a little bit about why I’m really excited to be at the Company now, just a bit over two months.

Before joining Affimed, I’ve held senior roles in research and development, most recently at Kymab in Cambridge, UK as Executive Vice President and Head of Research and Development, responsible for building a growing pipeline of 15 proprietary drug candidates, which included antibody programs in oncology. I’ve also held the roles of Chief Development Officer at MorphoSys AG in Munich, Germany and developing there the portfolio of proprietary therapeutic antibody programs in cancer and immunology, and a few years back, the role of Director of Immunology, Tissue Growth & Repair Early Development at Genentech, where I oversaw all preclinical development programs, including a number of IND submissions in immunology early development. I have a habilitation in Experimental Internal Medicine from Ludwig Maximilian University of Munich, where I also lecture in early drug development.

While I knew Affimed from before, I was really happy to find out about the substantial progress the Company has made when the opportunity to join presented itself, and I am now even more excited about the highly differentiated platform and programs. As someone personally touched by cancer — sadly, my brother-in-law recently passed away of melanoma at the age of only 52 — I have intimately witnessed the shortfalls of treatment, and I’m greatly motivated by our unique approach to giving patients back their innate ability to fight cancer. The innate immunity opportunity is largely untapped, and the work that the Company is doing in this exciting area was one of the key drivers in my decision to join Affimed. The Company’s proprietary ROCK platform holds the promise to really deliver meaningful and transformative medicines to cancer patients in need of better therapies. I’m thus really looking forward to bringing my experience and ideas and working with the talented team at the Company and to be here.

Now, before we come to the AACR posters, let me take a few minutes to share my excitement about our overall scientific approach. Innate immunity represents the first line of defense to maintain the integrity of our body and to protect us against viral infections, parasites and cancer. Immunosurveillance of these threats by innate immunity is highly efficacious, as demonstrated for example by our protection from cancer over decades. However, malignantly transformed cells sometimes evolve and escape mechanisms to bypass innate immunity, leading to cancer. Therefore, activating innate immunity is a promising strategy to treat cancer.

And I’m now coming to Slide 7. Major effects — major effector cells of innate immunity are natural killer or NK cells and macrophages. Activation of NK cells is regulated tightly by a balance of signals from inhibitory receptors, recognizing ligand on healthy cells and by activating receptors recognizing ligands that are stress-induced on disease cells, like for example, tumor cells. Therefore, NK cells are specialized to differentiate between healthy tissues and a tumor lesion, which is a major challenge for T-cell-based immunotherapies and demonstrated by severe adverse events related to cytokine release syndrome or neurotoxicity shown by this class of drugs. By contrast, NK cell-based therapies, including adoptive cell — transfer of NK cells from a healthy individual to a cancer patient are well-tolerated with a low degree of toxicity. Overall, actualizing this untapped potential of the innate immune system in fighting cancer has recently gained real interest. In particular, the MD Anderson CAR NK data in DLBCL demonstrated this potential. We are one of the leaders in this space with our bispecific innate cell engagers, and I would now like to briefly explain the unique design elements of our ICEs, innate cell engagers.

Slide 8: as you see here, Affimed’s ICEs are tetravalent bispecific antibodies with two binding moieties, the single-chain Fv domains for each the tumor antigen and CD16A on NK cells and macrophages.

Slide 9: these are made from Affimed’s ROCK or Redirected Optimized Cell Killing platform, which offers unique engineering opportunities to build customized ICEs with tailored binding affinities, tailored scaffolds and tailored pharmacokinetic and pharmacodynamic profiles. A key element of these ICEs are the proprietary single-chain Fv domains recognizing and triggering CD16A on NK cells and macrophages via binding to a unique epitope on CD16A far apart of the binding side of conventional antibodies. By binding on CD16A, on natural killer cells and macrophages and on the tumor antigen on cancer cells, our innate cell engagers first establish a bridge between innate immune cells and tumor cells. By contrast to conventional monoclonal IgGs, binding of Affimed’s ICEs to CD16As occurs with a roughly 1,000 fold higher affinity to both the low and the high affinity [Indecipherable] variance of CD16A without being prone to plasma IgG competition, and thus significantly broadening the patient population, which might benefit from ICE-based therapies. Furthermore, the — Affimed’s ICEs are highly selective for binding to CD16A and not CD16B, restricting ICE’s stimulated activation to NK cells and macrophages, representing the predominant immune cell population, to express CD16A. This concept aligns well with the observed good safety profile of Affimed’s ICEs currently in clinical studies.

Let me now briefly explain how our ICEs are actually killing tumor cells on Slide 10. When the natural killer cells and tumor cells are brought together, natural killer cells release perforins to create pores in the tumor cell membrane through which granzymes enter the tumor cell, triggering apoptosis and resulting in tumor cell death. And this is called antibody-dependent cellular cytotoxicity, or ADCC. When macrophages and tumor cells are brought together by the ICE, the macrophages engulf and phagocytose the tumor cells, resulting in internalization and degradation of the tumor cell. This is called antibody-dependent cellular phagocytosis, or ADCP.

I’m now advancing to Slide 11. Through cross-talk via dendritic cells, we believe that the adaptive immunity can also be triggered as the second line of defense, leading to an overall concerted and strong anti-tumor response.

Let me now explain to you why we see such a good safety profile with our ICEs in preclinical studies. NK cells have a proven safety record based on only graft-versus-host reactions following autologous or allogeneic cellular transfer, representing a strong differentiator from toxicities observed with T-cell-based therapies. The reasons for this are manifold but are based on the particular immune biology of NK cells, which I briefly explained at the beginning of my section. NK cells express germline encoded activating and inhibitor receptors, which are distributed stochastically over the entire NK cell population of a given individual. These NK cells are licensed to kill once they encounter a matching target cell. However, only a fraction of the entire population of NK cells might express activating receptors matching the cognate ligands of the target cells.

Since roughly about 90% of NK cells found in peripheral blood express CD16A, the proportion of target receptive NK cells will change in the presence of Affimed’s ICEs, leading to increased efficacy to kill the target as demonstrated in preclinical and clinical studies with our current development programs. Despite this increase in efficacy of NK cells upon ICE stimulation, their target selectivity appears to remain unchanged based on the absence of on-target, off-tumor toxicities in clinical studies and preclinical studies in non-human primates.

Learnings from these studies imply that NK cells are kept in check by a predominance of inhibitory signaling upon encounter with healthy cells, expressing target antigens, even in the presence of Affimed’s ICEs. The situation is very different in a tumor lesion. Here, the elevated levels of the target antigen, the induced expression of ligands of activating NK cell receptors and gradients of chemokine attractants are regarded as important factors to target ICE-stimulated ADCC and ADCP to the tumor lesion, while sparing healthy tissue. This very tolerable preclinical safety profile of ICEs has now been demonstrated in three ICEs, and most recently, in the anti-BCMA ICE program, formerly called AFM26, we licensed to Genentech, and our anti-EGFR ICE program, AFM24.

In contrast to the lack of any toxicity observed with our AFM24 in non-human primate studies, approved anti-EGFR antibodies, which block the signaling through the EGFR receptor, showed dose depending and severe toxicities, in particular in this sphere [Phonetic]. The promising safety profile of our ICEs would enable us to combine them with different approaches, including, for example, adoptive NK cell transfer or the combination of checkpoint inhibitors.

Having said all that, let me now highlight data from the two e-poster presentations at the Virtual Meeting of the American Association of Cancer Research, and we’ll start with AFM24 on Slide 12. So, the first poster presentation of AFM24, a bispecific EGFR/CD16A innate cell engager, has a mechanism distinctly different from EGFR signaling inhibition approaches.

Slide 13: the poster highlights the two main mechanisms of action of AFM24 antibody-dependent cell-mediate cytotoxicity, ADCC, and antibody-dependent cellular phagocytosis, ADCP, which holds the potential to benefit a broad set of patients with hard-to-treat EGFR-expressing cancers. Indeed, EGFR-expressing solid tumors represent one of the biggest challenges in terms of treatment modalities, and consequently, the unmet need for patients with EGFR-expressing tumors remains among the largest in oncology today.

The current EGFR targeting therapies work primarily through the inhibition of EGFR signaling. In contrast, AFM24 was designed to activate innate immunity to kill tumor cells, leveraging our CD16A binding paratope. Our AFM24 simply uses EGFR as a docking site. The molecule then establishes a synapse between the tumor and innate immune cells such as NK cells and macrophages, which initiates ADCC and ADCP.

In the poster, we show AFM24 mediated ADCC and ADCP in a number of cell lines, including those with KRAS such as the 12 C to G KRAS mutation and/or BRAF mutations. For us, this confirms that AFM24’s potency is unaffected by mutations in the EGFR signaling pathway, which can lead to resistance for therapy and negatively impact the prognosis of patients. Given AFM24’s mechanism, there’s preclinical rationale to support AFM24’s potential to provide benefit to a broad range of patients. In addition, AFM24 has demonstrated the ability to induce ADCC and ADCP in cell lines, which have a low EGFR density on their surfaces, where it still induces strong ADCC and ADCP mediated cell killing, even at low effector to target ratios.

We indeed designed AFM24 to show substantially reduced EGFR signal inhibition, which provides the scientific rationale that AFM24 could demonstrate an improved safety profile versus other EGFR targeted approaches. The preclinical proof point is the pharmacology, toxicology study at cynomolgus monkeys, confirming our hypothesis. AFM24 was well tolerated in its 28-day GLP toxicology study up to the highest dose of 75 mgs/kg. In addition, we observed half-life of AFM24 in cynomolgus is within IgG-based comparators. In the meantime, we’ve started dosing patients and address or tell you more about our first clinical experiences.

Advancing to Slide 14, moving on to the Genentech-Roche program, RO7297089, which is previously AFM26, poster, which focuses on the preclinical pharmacology and safety of the anti-BCMA innate cell engager that we partnered with Genentech. As this is a Genentech-owned asset, I thought I would just focus on the key highlights on Slide 15. RO7297089 shows potent cell killing in tumor cell lines employing NK cells as effector cells. Unlike T-cell engagers, the minimal increase in cytokine suggests a low-risk of cytokine release syndrome. A four-week safety study in cynomolgus showed a favorable safety profile with no cytokine release or adverse findings observed in both tested dose levels, which were 15 and 50 mgs/per kg. The time and dose-dependent reductions in serum IgG levels and plasma cell markers, which are BCMA and the J chain mRNA, were observed, suggesting the selective killing of BCMA positive cells by engaging CD16A positive immune cells.

On clinicaltrials.gov, Genentech posted a first-in-human Phase I open-label multi-center global dose escalation study designed to evaluate the safety, tolerability and pharmacokinetics of RO7297089 in patients with relapsed or refractory multiple myeloma. The study appears to open for recruitment soon.

Taking together, the two AACR posters show encouraging preclinical efficacy, combined with a promising safety profile, providing a strong rationale for further clinical development, underscoring the potential of our ROCK platform. We’re also broadening our early-stage pipeline with additional innate cell engagers from our ROCK platform. As Adi already mentioned, our two new CD16A binding innate cell engager candidates, AFM28 and AFM32, are moving along well towards later stage preclinical development.

I will now turn the call over to Andreas, who will provide the key clinical updates.

Andreas Harstrick — Chief Medical Officer

Yeah. Thank you, Arndt, for this really comprehensive overview of the NK cell biology and technology, which I think shows why we are very excited here at Affimed to work on this technology on these molecules, and for my part, having the opportunity and the privilege to guide these molecules towards clinical development and through the clinical development. Also a warm welcome to everybody who joined on the phone today.

Before I go into the details of our clinical programs, let me make a couple of introductory remarks. As Adi already mentioned and as you are all aware of, we are still in the middle of the COVID-19 pandemic, which continues to pose unprecedented challenges for the conduct of clinical trials. Having said that, we have been in very close contact with our participating institutions and with our investigators in order to ensure and to optimize how we can make our novel therapies accessible to patients who are in dire need for additional treatment options. The guiding principles here have not changed compared to what we discussed in March. So, patient safety is our utmost concern and is observed in all things that we do, as well as the integrity of the data, which again is in line with the recommendations that were given by competent authorities.

Now, if you can move to Slide 17 and start with our first program, AFM13, the CD30/CD16A engaging ICE, and I would like to focus on two programs here, the AFM13-202 or the REDIRECT trial. This is our registration targeted trial in patients with peripheral T-cell lymphoma, who have exhausted all standard of care therapies. This trial is progressing despite COVID-19. Compared to the update in March, we were able to add additional sites and open additional sites for this trial. So, we now have 47 active sites contributing patients around the globe. And on a site level, we do see a stable recruitment of patients.

If we move to our second program, AFM13-104, this is our collaboration effort together with investigators at MD Anderson Cancer Center. And the scope of this study is to combine AFM13 with cord blood-derived national [Phonetic] killer cells. This program has completed all necessary steps in order to be ready for patient recruitment, including FDA validated — mandated validation runs of the cord blood-derived NK cell product. So basically, everything is in order to enroll patients. But as you know, Texas is one of the regions where we still see an increase in COVID-19 cases. And as a consequence, the clinical operations at MD Anderson have been [Indecipherable] significantly. So we are monitoring the situation here, but we are depending on a relief or a lift of some of the restrictions due to COVID-19 at MD Anderson to be able to enroll first patients.

If we move then to AFM24, and we can go to Slide 19, AFM24 is, as Arndt has elaborated on, our second molecule targeting EGFR and CD16A. And as you may recall from my introduction three months ago, as somebody who has spent basically close to 20 years of his career to work on EGFR targeted therapies, having been responsible for the medical programs of Erbitux as well as Portrazza, for me, this is an absolutely exciting program as due to this very innovative and unparalleled mechanism of action, I think we have a compound here that can target very difficult to treat population of patients with EGFR expressing tumors and addressing a lot of the shortcomings and limitations of the currently available EGFR targeting therapies.

As we have disclosed last week, we were successfully initiating our clinical trial sites. In fact, we have now three active sites, two in the US, one in Spain, that could contribute patients. And we are very confident to get our final and fourth site onboard within the next couple of weeks. We also were able to successfully dose the first two patients in Cohort 1 of our dose escalation study. We have not observed dose-limiting toxicities, and in accordance with the recommendations given by the independent data safety monitoring board, we have opened Cohort 2, which now is open for patient recruitment.

So with this, I would conclude my short summary of our clinical programs and would hand over to Michael, who will give you an update on our financial situation.

Michael Wolf — Head of Finance

Okay. Thank you very much, Andreas. Affimed’s consolidated financial statements have been prepared in accordance with IFRS as issued by the International Accounting Standard 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.

As Adi already mentioned, we ended the first quarter with EUR88.2 million in cash, cash equivalents and current financial assets as compared to EUR104.1 million as of December 31, 2019. In addition, the Company raised net proceeds of EUR18.8 million under its ATM program. The pro forma cash position of the Company as of March 31, 2020, including the net proceeds from the ATM, would be EUR107 million. This cash infusion is planned to be used to help support a broader development strategy for AFM24.

Based on our current operating plan and budget assumptions, we anticipate that our cash position will enable us to fund our planned clinical development and early development activities well into the first half of 2022. Net cash used in operating activities for the three months ended March 31, 2020 was EUR16.5 million compared to EUR13.4 million in the first quarter of 2019, primarily due to higher cash expenditure for research and development efforts.

Total revenue for the first quarter of 2020 was EUR5.1 million compared to EUR11.4 million in the first quarter of 2019. Revenue in 2020 and 2019 predominantly related to the Genentech collaboration with EUR4.8 million in 2020 and EUR10.6 million in 2019. Revenue from the Genentech collaboration in the first quarter 2020 was comprised of revenue recognized for collaborative research services performed during the quarter.

R&D expenses for the first quarter of 2020 were EUR11.4 million compared to EUR8 million for the first quarter of 2019. The increase was primarily related to higher expenses for the AFM13 registration directed study in pTCL, manufacturing activities for AFM13 clinical study material, and early-stage development and discovery activities.

G&A expenses for the first quarter of 2020 were EUR3.5 million compared to EUR2.4 million in the first quarter of 2019. The increase is primarily related to higher personnel expenses, higher SOX compliance costs, legal, consulting and audit costs.

Net loss for the first quarter of 2020 was EUR8.3 million or EUR0.11 per common share. For the first quarter of 2019, the Company’s net income was EUR1.9 million or EUR0.03 per common share. Weighted number of common shares outstanding for the quarter ended March 31, 2020 were 76.2 [Phonetic] million.

I would like to turn the call back over to Adi for closing comments before we open the call for questions. Adi?

Adi Hoess — Chief Executive Officer

Thank you, Michael, Arndt and Andreas. As we close today’s prepared remarks, half way into 2020, Affimed is continuing to make progress on several fronts. The data presented at AACR shows that our innate cell engagers are consistent in their ability to induce potent killing in tumor cell lines and low target expression in the relevant preclinical models and appear to have promising differentiated safety cohorts. For AFM24, we are now actively recruiting into the second dose cohort. [Indecipherable] BCMA innate cell engager, Genentech recently posted a clinical trial [Indecipherable] first-in-human Phase I study. Recruitment according to the site is expected to open soon.

On AFM13, recruitment into the pTCL study is ongoing, and we continue to be successful in bringing on new sites. Regarding the combination of AFM13 with cord blood-derived natural killer cells, we are proceeding with the planned initiation of an investigator-sponsored trial at MD Anderson Cancer Center.

Our ROCK platform has generated two novel and [Indecipherable] preclinical molecules. We have a good cash position, which allows us to pursue our program, and as shown on Slide 20, to potentially yield — meet multiple value drivers in 2020 and 2021. And most importantly, we have strengthened our management team with now the addition of industry experts, including a new Chief Financial Officer, who will be joining us next month.

Before I open the session for the Q&A, I would like to reiterate our appreciation for the unwavering commitment of our employees and our gratitude to our investigators and clinical advisors, and most importantly, the patients and their families who are continuing their strong support during this very difficult period.

We would now be happy to take any questions that you may have. Operator? Thank you.

Questions and Answers:

Operator

[Operator Instructions] Your first question comes from the line of Maury Raycroft from Jefferies. Please ask your question.

Maury Raycroft — Jefferies — Analyst

Hi, good morning, everyone, and thanks for taking my questions and congrats on the update today, too. So, just checking for AFM13 timelines for the registrational program, if you could provide any more clarity on timelines? And should we expect an initial update in first half of ’21?

Andreas Harstrick — Chief Medical Officer

Yeah. This is Andreas. I can take this question. As I said in my introductory remarks, COVID-19 still makes planning a little bit of a challenge. We have unprecedented factors. We are encouraged in what we are seeing in terms of recruitment in our sites. So, we anticipate to have interim data around the middle of 2021.

Maury Raycroft — Jefferies — Analyst

Got it. Okay. And then, you mentioned progress with AFM13 plus the cord blood NK cell combo study with MD Anderson, where you completed their required validation work for the stable AFM13 plus NK cell premix. I guess, can you provide more specifics on the complex stability? And just wondering when this is eventually commercialized, would it be a frozen down mix? Or would you tie [Phonetic] the cells first, add in AFM13 and then administer? Could you just provide more clarity on that if possible?

Andreas Harstrick — Chief Medical Officer

Adi, I think it’s question for Wolfgang.

Wolfgang Fischer — Chief Operating Officer

Hi, this is Wolfgang. Maury, it’s difficult to say at the current time how our commercial product would look like, whether it’s a premix product, or whether it’s a co-administration [Indecipherable]. We first need to do this study to have the proof-of-concept and to see how it works out. So, I think it’s too early to say how this should look like.

Maury Raycroft — Jefferies — Analyst

Got it. Okay. And for — I guess, last question on AFM24. You guys reported you’re not seeing any safety issues or efficacy in Cohort 1. I guess, can you comment on any Pb biomarker activity at this point? And do you still expect to see activity in Cohort 3?

Andreas Harstrick — Chief Medical Officer

So the data that we released were very fresh. So we have not seen those limiting toxicities, and that was the reason why the data safety monitoring committee recommended the opening of Cohort 2. Now, we’re collecting pharmacodynamic markers, as well as other biomarkers through the course of the study, but we have not completed the analysis of these markers yet. Again, I think, it is premature to speculate which will be an effective dose level. I think it’s fair to say that dose level one was a very low dose. So here, the starting dose level was really chosen to maximize safety. And I think we will learn more about the pharmacokinetics and pharmacodynamics as we continue to enroll patients in the additional dose levels.

Maury Raycroft — Jefferies — Analyst

Got it. That’s helpful. Okay. Thanks again for taking my questions.

Operator

Your next question comes from the line of Jim Birchenough from Wells Fargo. Please ask your question.

Jim Birchenough — Wells Fargo — Analyst

Hi, guys. Thanks for all the detail on the call, and congrats on all the progress. I guess a few questions. First for Andreas. For the two first patients in Cohort 1 that were recruited, Andreas, could you talk a bit about those patients, what tumor types and whether they were having [Phonetic] any specific markers, KRAS markers, that sort of thing? Any detail you can give on those first two patients?

Andreas Harstrick — Chief Medical Officer

We have not disclosed all the details. What I can say is that these two patients had probably the two most predominant tumor types, so non-small cell lung cancer and colorectal cancer. We have not collected all information on the KRAS mutation status yet. But as I said, the first dose level was really maximized or targeted to establish safety and is probably well below where we would expect to see pharmacodynamic activity.

Jim Birchenough — Wells Fargo — Analyst

And Andreas, can you remind us, are you taking pre and post treatment biopsies? And is there any ability to look at NK cell recruitment or infiltration to the tumor?

Andreas Harstrick — Chief Medical Officer

The protocol provides the option to have pre as well as on-treatment biopsies. These are not mandatory. So, they are on a voluntary basis. And we will see how many biopsies we will get as the trial moves along. But as we have very committed investigators, this is one of the exploratory endpoints we are looking into.

Jim Birchenough — Wells Fargo — Analyst

Got it. And then, maybe just for Arndt. Arndt, you anticipated our question on how you’re able to spare healthy tissue that express EGFR and avoid on-target off-tumor effects. Can you measure those inhibitory signaling, any biomarkers of inhibitory signaling that’s protective to normal tissue? I guess, number one.

Adi Hoess — Chief Executive Officer

Yeah. We may have lost Arndt. Arndt, are you on mute? Otherwise I am handing over…

Arndt Schottelius — Chief Scientific Officer

Yeah. Sorry, I was on mute. Apologies. So Jim, yes, so indeed, one could measure those markers. No, we haven’t measured them in the [Technical Issues]. But of course, the concept is clear because it’s ubiquitous for NK cells. It may be interesting, as Andreas said, when we look at some of those patients, which may have — where we may have biopsy data. Of course, we will also have a closer look at those NK cells and potentially the presence and absence of activating inhibitory ligands.

Jim Birchenough — Wells Fargo — Analyst

And then Arndt, you gave a pretty thorough overview of NK cell biology. Can you comment on whether there’s dysregulated NK cell function in cancer, something that impairs NK cell ability to survey and eliminate emerging cancer cells? And is there something about an innate cell engager that overcomes that?

Arndt Schottelius — Chief Scientific Officer

We have something — really interesting question, Jim. It’s something not really well studied. Of course, we know that there is overall, also in the elderly and frail, of course, a dysfunctional system. There are quite a few reports in that direction. I don’t think it really has evolved as a strong picture in terms of providing them different patient populations. But again, it’s something we want to learn more as we further advance those programs and get biopsies and do the comprehensive accommodating studies to look at that.

Jim Birchenough — Wells Fargo — Analyst

Great. And then just finally, Adi, I might have missed it on the call. Was there an update on the progress with the BCMA engager with Genentech and progress to IND in first patient dosing? Or did I misconstrue or something else you were saying?

Adi Hoess — Chief Executive Officer

Yeah, I’ll hand this question over to Arndt, again.

Arndt Schottelius — Chief Scientific Officer

Yeah, Jim, so indeed, we did talk about the poster, which of course the — means everything is poised to enter the clinic, and we did say, based on the posting clinical trials [Indecipherable], it’s up and running. The Phase I is described, dose escalation, pharmacokinetics, usual Phase I that — we would expect that to start some time probably in July.

Jim Birchenough — Wells Fargo — Analyst

Perfect. Well, thanks for taking the questions, guys.

Arndt Schottelius — Chief Scientific Officer

Thank you.

Operator

Your next question comes from the line of Yale Jen from Laidlaw & Company. Please ask your question.

Yale Jen — Laidlaw & Company — Analyst

Good morning, and thanks for taking the questions. This is a very comprehensive overview of the NK cell and macrophage engagement in cancer. The first question is that have you guys talked any — in terms of AFM24, any data update, maybe the initial data update toward the end of this year? Or it’s too — still too early to suggest that?

Andreas Harstrick — Chief Medical Officer

Yeah. I think it’s too early to give an exact guidance. We will monitor safety closely, and I think we will give updates as we did — as we move through the dose escalation cohorts. Now as it is, I think, characteristic or typical for Phase I studies, you do not really know how many dose cohorts you will need to reach your pharmacodynamic active dose and then your recommended Phase II dose. So I think the disclosure of additional data depends quite a bit on the number of dose escalation steps needed. But as I said, we will update on the progress of the study as we go along.

Yale Jen — Laidlaw & Company — Analyst

Okay. Great. That’s very helpful. Maybe two more quick questions. The first one is, for the Genentech studies, I noticed that in the clinical data, most of the clinical sites are in Northern Europe or in Australia. Is that because maybe based on the inclusion or exclusion, particularly the exclusion criteria, those areas — those sites being some — geographic sites being selected may be more, I guess, appropriate to getting the eligible patients?

Arndt Schottelius — Chief Scientific Officer

Yeah, I’ll take that question. Adi, do you want to go or…

Adi Hoess — Chief Executive Officer

Yeah. I just want to say, we have nothing involved in the planning of the clinical study. So indeed, we cannot truly comment on the basis of their choices, but we know that they intend to file an IND as well. So that’s all the information we have. Arndt, do you want to add to this?

Arndt Schottelius — Chief Scientific Officer

No, it’s just that, as you said, we can’t really comment in detail. I just think it’s more appropriate to talk to Genentech. Thank you. It’s a good question, Yale.

Yale Jen — Laidlaw & Company — Analyst

Okay. Maybe the last one here is that it’s more theoretical on both basic science, which is that your ICEs have been able to engage in both macrophage and NK cells. The question is that, can you guys sort of fine-tune the system to gear for either one of the two? Or how — or whether you have a way to assess which type of cells, either — the effector cells has played a greater role at any sort of particular circumstances?

Arndt Schottelius — Chief Scientific Officer

Yeah, really interesting question. I’d be glad to take it, yeah. So, really interesting question. I think the straight answer is, it’s really not intended to fine tuning, Yale, because we want both parts. They play both a significant part, ADCC and ADCP. And as I laid out in the introduction, the CD16A expression is really predominantly NK cells and macrophages, for example, not on neutrophils like CD16B. So we already have a high specificity, and we want that specificity, so we get the tumor killing by the most effective killer cells. So coming back to your question, there is no intent to fine-tune the one or the other direction. However, we are looking very detailed to understand exactly what’s happening. While ADCC, for example, is quite well looked at, ADCP is still more of an open field, and we are doing really translational research and working with great academic partners to understand that in more detail.

Yale Jen — Laidlaw & Company — Analyst

Okay. Great. Thanks. And again, congrats on the progress in this tough time.

Arndt Schottelius — Chief Scientific Officer

Thank you.

Operator

Your next question comes from the line of Ike Oji from BMO Capital. Please ask your question.

Ike Oji — BMO Capital — Analyst

Hi, everyone. This is Ike on for Do Kim. Thanks for taking my question, and congrats on the progress. Just a quick one on your early [Phonetic] pipeline with AFM28 and AFM32. Do you know when we’ll be able to kind of get some data on there from a preclinical standpoint potentially and around when will we see it actually enter into the clinic? That would be helpful for us. Thanks.

Adi Hoess — Chief Executive Officer

Arndt, do you want to take that?

Arndt Schottelius — Chief Scientific Officer

Yeah. Sure, will be glad. So, yes, a good question. To be consistent with our previous updates, they’re making — 28 and 32 are making good progress towards late preclinical stage. And we had kind of guided approximately towards the end of 2021 for an IND filing for 28. 32 is further behind. So, of course, pretty, I think, clear to you, from today’s perspective, we can’t be really exact, but that’s what we are currently targeting.

Ike Oji — BMO Capital — Analyst

Okay. Thank you for that and see you at the conference.

Arndt Schottelius — Chief Scientific Officer

Thank you.

Alexander Fudukidis — Head of Investor Relations

Thanks a lot. See you later. Thanks so much. See you later. Thank you so much. So this concludes our update call of the first quarter financial results and project update. Appreciate your attendance and the many questions, and we look forward to progressing further. Thank you so much.

Operator

[Operator Closing Remarks]