During the Affimed (NASDAQ: NASDAQ:AFMD) second quarter 2024 earnings and corporate update call, the company highlighted significant clinical progress with their innate cell engagers, particularly in treating non-small cell lung cancer, Hodgkin lymphoma, and acute myeloid leukemia.
The new CEO, Shawn Leland, emphasized the potential of these programs and the company's focus on securing funding to advance them. Affimed reported a cash reserve of €34.4 million, sufficient to fund operations into the second half of 2025, despite a net loss of €15.5 million for the quarter.
Key Takeaways
- Affimed's clinical trials show promising results for their therapies in treating various cancers.
- The company has a strong cash position, expected to last until the second half of 2025.
- CEO Shawn Leland is prioritizing funding and investor engagement for advancing clinical programs.
- Encouraging efficacy data for AFM24 and AFM28 in treating non-small cell lung cancer and acute myeloid leukemia, respectively.
- Plans to expand cohorts and explore strategic partnerships for further development.
Company Outlook
- Affimed intends to provide additional data on their clinical programs in Q4 2024.
- The company is exploring strategic options, including partnerships, to advance their clinical programs.
- Regulatory discussions and data will guide the potential market approval strategy.
Bearish Highlights
- Affimed reported a net loss of €15.5 million for the quarter.
- The company is dependent on securing additional funding to continue their clinical programs.
Bullish Highlights
- Promising clinical results could lead to successful therapies and market approval.
- Strong cash position provides a runway for continued operations and research.
- Potential for combination therapies to provide more effective treatment options.
Misses
- No updated PFS data was provided during the call; however, the company noted that the data will be available in Q4 2024.
Q&A Highlights
- The company discussed the potential for deeper and more durable responses with combination therapies.
- The response rates for AFM28 in AML are encouraging, especially given the high rate of complete responses.
- Affimed is considering expanding cohorts based on the data and is evaluating the best path to market approval.
Affimed's clinical programs show promise in treating cancers with few existing treatment options, particularly in EGFR mutated cohorts. The company's focus on precision oncology and combination therapies aligns with current trends in the field. With a solid cash position and strategic planning, Affimed is poised to further develop their clinical programs and explore market approval pathways, pending regulatory discussions and additional data.
InvestingPro Insights
Affimed (NASDAQ: AFMD) has been navigating through a challenging financial landscape, as reflected in the real-time data from InvestingPro. With a market capitalization of $57.94 million and a negative P/E ratio of -0.64, investors are closely monitoring the company's performance metrics. The negative P/E ratio, which remains consistent when adjusted for the last twelve months as of Q2 2024 (-0.67), suggests that the market is skeptical about the company's current profitability.
InvestingPro Tips indicate that while Affimed holds more cash than debt on its balance sheet, there is a concern about the company quickly burning through cash. This aligns with the company's report of a net loss of €15.5 million for the quarter. Moreover, analysts anticipate a sales decline in the current year and do not expect the company to be profitable this year. These factors are essential for investors to consider, as they may impact the company's ability to sustain operations without additional funding.
The price of Affimed's stock has been under pressure, having fallen significantly over the last three months. This is corroborated by a 39.94% drop in the three-month price total return, which is a critical metric for investors tracking short-term performance.
For readers interested in a deeper analysis, there are over 9 additional InvestingPro Tips available at https://www.investing.com/pro/AFMD, offering further insights into Affimed's financial health and market position. These tips could provide valuable context for investors trying to understand the potential risks and opportunities associated with the company's stock.
Full transcript - Affimed NV (AFMD) Q2 2024:
Operator: Good day, everyone, and welcome to Affimed Second Quarter 2024 Earnings and Corporate Update Call. At this time, all participants are in a listen-only mode. [Operator Instructions] As a reminder, today's conference call is being recorded. I would now like to introduce your host for today's call, Alex Fudukidis, Head of Investor Relations at Affimed. Please go ahead.
Alex Fudukidis: Thank you, Olivia, and thank you all for joining us today for our second quarter 2024 update call. Before we begin, I'd like to remind everyone that we issued the relevant press release earlier today, and that can be found on our Investor Relations section of the website. On our website, you can also find the presentation we will be using today. On the call today, we have members of our management team, including Shawn Leland, our new Chief Executive Officer; Andreas Harstrick, our Chief Medical Officer; Wolfgang Fischer, our Chief Operating Officer; Denise Mueller, our Chief Business Officer; and Harry Welten, our Consulting Chief Financial Officer. Our financials today will be presented by our VP of Finance, Michael Wolf. The team will be available for Q&A after the prepared remarks. Before we start, I would like to remind you that today's presentation 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 these 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 Forward-Looking Statements in the press release that we issued today and filed with the SEC. With that, I'll turn the call over to Shawn. Shawn?
Shawn Leland: Thank you, Alex, and good morning, everyone. I'm excited to speak with you today as the new CEO of Affimed. Although I am only a few days into this role, I am eager to share my initial thoughts with our shareholders and the financial community. My decision to join Affimed was data-driven. After thoroughly reviewing Affimed's portfolio of innate cell engagers, I am impressed with the platform and firmly believe we are on the verge of something transformational. The commercial potential is quite significant as we have achieved clinical proof of concept across three assets, each with distinct indications. This progress is particularly encouraging for the many advanced refractory or relapsed patients who have limited options across indications such as non-small cell lung cancer, Hodgkin lymphoma, and acute myeloid leukemia. Importantly, Affimed's diverse clinical portfolio offers valuable strategic options for our business and, from my perspective, is an enviable position in the biotech world. My immediate commitment to you, our shareholders, is to hit the ground running and to secure funding to support our promising clinical programs. I look forward to engaging with our current shareholders and prospective investors alike. I will be speaking with those already familiar with the current Affimed data and new investors to share my enthusiasm over the clinical pipeline poised for numerous data readouts in the next 12 to 24 months. Although the capital markets have been challenging to biotechs in 2024, I am confident our compelling clinical data differentiates us and will allow us to further extend our runway. Additionally, I am energized to thoroughly examine our business development strategy and broaden our relationships with pharma partners. Innovation is at the heart of our industry and I am particularly interested in exploring how creative partnering approaches can advance our clinical development, broaden our clinical development strategy to reach more patients faster, and expand patient access to our therapies. During the interview process, I was impressed with Affimed's passionate employees and culture: dedicated to developing life-changing therapies to address underserved patient populations. To both survive and thrive, we must achieve operational efficiency and excellence. While I acknowledge the significant organizational changes Affimed has undergone over the past year, I am committed to continuous improvement and a growth mindset to ensure we are consistently delivering meaningful value to our key stakeholders. Before I turn the call over to Andreas, I want to express my sincere thanks to him and the role he served as acting CEO over the past several quarters. Now, over to you, Andreas.
Andreas Harstrick: Yeah. Thank you, Shawn, and I'm really happy to have you on board. And also good morning to everybody who is listening on to our call. Let me go through our programs in detail and put some new data in perspective. We are happy to report that we again have made progress in all programs. I will start with our AFM24-102 trial, in which we evaluate the combination of AFM24 plus atezolizumab in patients with non-small cell lung cancer who have failed standard of care options. Both the EGFR wildtype and the EGFR mutant non-small cell lung cancer cohorts are almost fully enrolled now. Today, we will share with you early efficacy data for the EGFR mutant cohort. As you know, the treatment sequence for patients with EGFR mutant non-small cell lung cancer starts with the application of an EGFR-specific TKI. Most patients today will receive third generation TKIs. While these treatments are highly effective in prolonging time to tumor progression, they are not curative for patients with advanced or metastatic disease and, ultimately, almost all patients will progress. Treatment options after failure to EGFR-specific TKIs are limited. Platinum-based chemotherapy is standard, but may in the future be replaced by a combination based on amivantamab and chemotherapy with or without lazertinib. While amivantamab containing regimens have shown some improvement over chemotherapy alone, they are also not curative and all patients will ultimately experience disease progression. If you look at the NCCN guidelines, there are no established treatment alternatives for EGFR mutant non-small cell lung cancer patients who have failed two lines of treatment. The options given by NCCN are either palliative care or single-agent chemotherapy, which is usually associated with low response rates and a progression-free survival of around four months or the enrollment into a clinical trial. And it's exactly these patients who currently have no treatment options available that we have enrolled into our study. As shown on Slide 4, a total of 24 patients have received treatment so far. Seven patients are not evaluable according to RECIST, including four patients who deteriorated rapidly, often within the first week on study. These are, for the most part, patients who had a long interval between the screening evaluation and the actual start of trial medication. And we have to assume that they had rapid tumor progression in the treatment-free interval. One patient did not have a follow-up scan and two patients are in the first two cycles having no tumor assessment yet. On Slide 5, you can see the patient characteristics. The median number of previous lines of therapy is 3. All patients have been pretreated with EGFR-targeting TKIs and the vast majority, more than three quarters, had also platinum-based combination chemotherapy. Only two patients had been pretreated with checkpoint inhibitors, reflecting the general belief in the medical community that EGFR mutant non-small cell lung cancer is not responsive to checkpoint inhibitors. On Slide 6, we show that in the 17 patients that are response-evaluable, we have four patients with an objective response, including one patient with complete response and three patients with partial response, all confirmed by sequential CT scans. And eight patients with stable disease, including patients with reductions in tumor volumes that failed the PR threshold, resulting in an objective response rate of 23.5% and a disease control rate of 70.6%. Importantly, the responses appear to be durable and thus clinically meaningful. All four responders were on treatment for at least seven months. Important to note, eight of 17 patients are still on treatment with a median follow-up for the cohort of over seven months. While these data are still early, they indicate like the data in the EGFR wildtype cohort, which we reported earlier this year, that a combination of AFM24 with a checkpoint inhibitor has activity in treatment refractory non-small cell lung cancer patients. It may become a meaningful treatment alternative for patients who failed standard of care therapies. It's worthwhile noting that these data are achieved with a regimen that does not contain any chemotherapy, an important distinction from other treatments as chemotherapy is often difficult to tolerate by these heavily pretreated patients. Let us now move to our CD30-targeting ICE (NYSE:ICE) molecule AFM13 or acimtamig, that we are developing in combination with AlloNK in our registration-directed LuminICE-203 study in patients with multi-refractory Hodgkin's lymphoma. As you see from the study diagram on Slide 8, the initial part of the study consists of four cohorts that are designed to optimize the doses of acimtamig and AlloNK, respectively. Cohorts 1 and 2 are fully enrolled and all patients have at least one efficacy readout conducted by an independent response assessment committee. As you see on Slide 9, all patients were heavily pretreated, having exhausted all standard treatment options, including combination chemotherapy, brentuximab and PD-1 targeting checkpoint inhibitors. 50% of the patients had also failed stem cell transplant. Given that there are no treatment alternatives for these patients, shown on Slide 10, we observe a response rate of 83.3%, which I believe is outstanding. This includes six patients or 50% with a complete response and four patients with a partial response. It's important to note that three of the four partial response patients have not completed their full treatment yet and are continuing to receive additional cycles. In this context, it may be important to remember our experience from the MD Anderson trial, where one-third of the complete responses occurred at later cycles. On Slide 11, I'm also happy to report that cohorts 3 and 4, in which we test a higher dose of AlloNK product are almost completely enrolled with 10 of the planned 12 patients on treatment. Enrollment in cohorts 3 and 4 progressed according to the planned enrollment schedule and there were no dropouts of patients during screening. Furthermore, we have now 10 different sites across the whole USA that have actively treated patients on the study. We plan to disclose data from all four cohorts at an upcoming scientific meeting in Q4 2024. Finally, let's review the updated results of AFM28, our CD123 targeting ICE for the treatment of acute myeloid leukemia, as shown on Slide 13. In this study, we have escalated dosing through six cohorts up to 300 milligrams flat dose weekly. The treatment is very well-tolerated with infusion related reactions, mainly of low grade being the main side effect. At the two highest dose cohorts of 250 milligrams and 300 milligrams, we did not observe any dose limiting toxicities. And in 12 patients, only three patients had a Grade 2 infusion related reaction, responding in all cases to symptomatic treatment. There were no Grade 3 or higher IRRs. One patient experienced a short lasting self-limiting cytokine release syndrome of Grade 1. Infections are characteristic manifestation of acute leukemia and was seen in approximately half of patients we treated in the study so far. However, no infection was considered to be treatment related by the investigator. The clinical activity is displayed on Slide 14. In dose level 5 of 250 milligram AFM28, we saw one complete response, 17%, and five stable diseases in heavily pretreated patients. Of note, the patient with a complete response was in remission for more than five months. In dose level 6 at 300 milligrams AFM28, the number of complete responses has increased compared to the data that we reported in our Q1 earnings call. Now three out of six patients have developed a complete response, or CRi, respectively, for a complete response rate of 50%, indicating a possible dose response relationship. In addition, two of three remaining patients at dose level 6 have shown stable disease. These highly encouraging results have led to our decision to expand cohort 6 by additional six patients to confirm the monotherapy signal that we have seen in the study so far. We plan to give a further update on these data at an upcoming scientific conference. As we show on Slide 15, we believe further development of AFM28 in combination with other AML therapies or with cryopreserved allogeneic NK cells would allow us to address again an area of significant unmet medical need. In the seven major markets, we see over 14,000 patients per year who fail at least two lines of standard therapy and require a new treatment option. With this, I will close the overview of our clinical programs and hand over to Michael Wolf for a review of the financial data. Michael, please.
Michael Wolf: Thank you, Andreas. Balance sheet and income statement highlights are shown on Slides 17 and 18 of the presentation. A quick reminder that 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 prepared in euros. Since our financials are described in detail in the press release we issued this morning, I will only provide highlights on this call. We ended the second quarter with cash, cash equivalents and investments of €34.4 million compared with €72 million on December 31, 2023. Based on our current operating and budget assumptions, we anticipate that our cash and cash equivalents and investments, together with anticipated proceeds from the ATM program and the sale of AbCheck, will finance us into the second half of 2025. Net cash used in operating activities for the quarter ended June 30, 2024 was €16.5 million compared with €33.3 million for the quarter ended June 30, 2023. Total revenue for the quarter ended June 30, 2024 was €0.2 million compared with €1.4 million for the quarter ended June 30, 2023. R&D expense for the quarter ended June 30, 2024 were €11.7 million compared to €25.3 million in 2023. G&A expenses for the quarter ended June 30, 2024 were €4 million compared to €6.3 million for the quarter ended June 30, 2023. Net loss for the quarter ended June 30, 2024 was €15.5 million, or €1.01 per common share, compared with a net loss of €29.4 million, or €1.97 per common share, for the quarter ended June 30, 2023. Now, I'll turn the call back to Shawn for final remarks. Shawn?
Shawn Leland: Thank you, Michael. As you listen to Andreas' update on our clinical programs, I hope you share my enthusiasm about the robustness of our science and data, as well as the potential of our therapies to address significant unmet medical needs. For instance, on AFM24, the data generated to-date in both the non-small cell lung cancer EGFR mutant and wildtype cohorts are encouraging and supports our hypothesis that the combination of AFM24 and PD-1 targeting may act synergistically on the immunity cycle. It is remarkable that this can be achieved with a chemotherapy-free approach and we look forward to sharing additional data this year from the non-small cell lung cancer EGFR wildtype cohort in Q4 of 2024. For our acimtamig program, the patients enrolled in the LuminICE-203 study are critically ill with advanced disease and no remaining approved treatment options. Our impressive overall response rate of 83% is a strong indicator of the promise of our approach and, when considered in the context of approved products, our data is very compelling and a much more heavily pretreated patient population. I look forward to sharing additional results from this study soon as we near completion of enrollment in cohorts 3 and 4 in Q4 of 2024. We are encouraged by the AFM28 monotherapy. There is a clear and strong signal, which is the basis for the expansion of dose cohort 6 by adding another six patients. We continue to believe there is potential for higher response rates and perhaps greater durability and a combination development approach. Relapsed/refractory AML is a difficult disease to treat and there is much room for improving response rates given what's seen with currently approved therapies with CR/CRi rates in the range of 15% to 30%. While we need more data and durability, the data we are seeing here underpins my enthusiasm for this program. Before we open the call to questions, I would like to express my sincere gratitude to both the management board and supervisory board for entrusting me with this important role. Lastly, I want to reaffirm my commitment to you, our shareholders. I am dedicated to increasing shareholder value through the successful execution of our clinical development programs, achieving milestones, forging new partnerships, and advancing our transformative therapies closer to patients who need them most. With this, I thank you all for your attention, and we are happy to take any questions that you may have. Operator?
Operator: Thank you. [Operator Instructions] Our first question coming from the line of Maury Raycroft with Jefferies. Your line is open.
Maury Raycroft: Hi, good morning. I'll say welcome to Shawn, and congrats on the progress, and thanks for taking my questions. I'll start with one quick one on AFM24. For the new EGFR mutant data, just wondering if you're observing any differences among patients who had prior third-gen TKIs versus those who are getting first- or second-gen TKIs?
Shawn Leland: Hey, Maury. It's Shawn. Thanks for the question. Andreas, do you want to respond to Maury's question?
Andreas Harstrick: Yeah. So, good question, Maury. No, we have not seen any differences. In fact, when we look at our four responders, three of the four responders have been pretreated with third-generation TKIs. So, there is obviously no cross resistance or no lower response rate if a patient had had a third-generation TKI compared to a first- or second-generation TKI.
Maury Raycroft: Got it. Okay. That's helpful. And then, for the LuminICE study, just wondering if you can remind me what expectations are for the higher NK cell dose for cohorts 3 and 4. And are you seeing any biological efficacy or safety differences between the 200 mg and 300 mg doses for cohorts 1 and 2?
Shawn Leland: Yeah. Thanks, Maury. Andreas, do you want to respond to this question as well?
Andreas Harstrick: Yeah. So, for the acimtamig dose 200 milligram and 300 milligram, so far, we have not seen any differences in terms of response rate. So, this is equal across the two cohorts. In terms of the cohorts 3 and 4, as a reminder, we do use a higher cell dose here. This is a cohort that is currently in evaluation and enrollment. The early data that we see are very encouraging, but I think we just have to wait until the data across all the 12 patients have matured, which we will be able to disclose in Q4 2024.
Maury Raycroft: Got it. Okay. And when you do the update in the fourth quarter of this year, will you have the go-forward doses selected at that point as well?
Shawn Leland: Andreas, you want to...
Andreas Harstrick: Yeah. This would be the aim. If you look at the study protocols, out of the four initial cohorts, we will select two cohorts for continuation in Stage 1 of the Hodgkin lymphoma program. And as the data mature, we believe that we will be able to make a data-driven decision here.
Maury Raycroft: Got it. Okay. Thanks for taking my questions.
Shawn Leland: Thanks, Maury.
Operator: Thank you. And our next question coming from the line of Daina Graybosch with Leerink Partners. Your line is open.
Daina Graybosch: Hi. Thank you for the question. Welcome, Shawn, to Affimed. I wonder as you step back and look across these three programs, if you -- a question to Shawn and to Andreas, how you're considering your development strategy? I think I noticed a change in AFM28, whereas at the last update, the plan was to immediately find a partner to combine with NK cells. And now I heard something that was a little bit more ambiguous, more broadly thinking about combination partner. So, if you could comment on AFM28 and also whether you're considering different approaches for AFM24 as you move forward? Thank you.
Shawn Leland: Yeah. So, Daina, thanks for the question, as well as the welcome. Maybe I'll start and then turn it over to Andreas. I mean, I think as it relates to AFM28, I mean, if you think back to the last update we provided, right, we didn't have the data that we have in hand today. I mean, I think seeing the encouraging monotherapy activity with three out of six patients showing a CR or CRi is quite encouraging. I mean, I think it's important to note that in this relapsed/refractory setting, and keep in mind, most of these patients have seen three or more prior lines of therapy, to see a 50% CR/CRi rate as we are continuing on in dose escalation is quite encouraging when comparable therapies are typically showing a CR/CRi rate in the 15% to 30% range. So, I mean, I think, we're starting to see kind of this potential dose response relationship, which I think leaves us a bit more encouraged with the monotherapy activity. I think as we've seen with the acimtamig's program, we do think that there is additivity or synergy that exists, in particular with AlloNK cells. So, I mean, under that context, if we add AlloNK cell to AFM28, could we see deeper and more durable responses? I think there's the potential for that. But I think, first and foremost, we're highly encouraged by the monotherapy signal. And by adding these additional six patients, we'll be able to get a stronger sense of how encouraging that monotherapy signal is. But I'll pause here and see if Andreas has anything to add.
Andreas Harstrick: I think you covered AFM28 very well. Again, these are, as always, in clinical development data-driven decision. And I just want to emphasize, if somebody had told me when we started AFM28 that we will have a 50% complete response rate, I would have said, "Yeah, great, I take it." But these are just outstanding data. And I think we have the obligation to find the best way to bring this treatment to patients. This can be in combination with either standard of care drugs that are used in AML, it can be in combination with an NK cell product. So, there are clearly multiple options. And yeah, AFM28 has become for us a very interesting and very promising product. The same is true for AFM24. Again, non-small cell lung cancer, a very challenging disease, especially if patients are pretreated with at least two lines of therapy. Again, this is the case for both of the cohorts, EGFR wildtype, EGFR mutant. You don't have any standard of care treatments. And to see a consistent efficacy result, and I think this is the most important thing, that's not just one number that pops up, but you see consistency, you see objective responses in both cohorts, you see durable responses in both cohorts, again, something that we believe is highly encouraging, can really change the life of patients in need. And we will have to find the best way as an organization to move these programs forward to bring them to patients, whether this will be best done in a partnership or, to a certain extent, initially alone as an Affimed organization. We will have [indiscernible] we are evaluating all strategic options and -- but the most important thing is that we have data to build on. And yeah, that's where we are right now, and I just can't share my enthusiasm about this data. It looks really, really very promising.
Daina Graybosch: Maybe one follow-up on AML. Is there a durability of response threshold you guys would like to see to think about a potential single-agent path forward?
Shawn Leland: Yeah, it's a good question. Andreas, do you want to respond to Daina?
Andreas Harstrick: Yeah. I mean, responses, of course, have to be durable to be meaningful for our patients. In these heavily pretreated patients, any single agent that produces responses or progression-free survival that is in the range of six months, I think is meaningful, especially if this can be achieved with very low toxicity. And so, this would be, I think, a threshold for a single-agent development, but again, given the very good side effect profile and a very unique mechanism of action, I think we also have any multiple kinds of options for combination development either with standard of care drugs or as we mentioned already with allogeneic NK cells.
Operator: Thank you. And our next question coming from the line of Bill Jahangiri with Truist Securities. Your line is open.
Bill Jahangiri: Hi. Congrats on the progress, and welcome to Shawn. I'm on for Kripa. I had a follow-up question on AML. I was wondering if you guys could maybe give us a hint of some of the mutations at some of these AML patients harbor? Because, I know the response rates are different in different subsets, and regardless, your data is very impressive in the monotherapy so far, but any sort of color on that would be great.
Shawn Leland: Hey, Bill. Thanks for the welcome. Andreas, do you want to respond to Bill's question as it relates to mutations that we've seen thus far on patients treated with AFM28?
Andreas Harstrick: Yeah. So, we are currently combining and compiling and collecting all these data. What we see so far, it's a mixture, so we do not have unusual selection. I think it's probably quite representative for the mutation pattern that you see in a pretreated AML population. And we will have all these data ready for our upcoming data release at a scientific conference in Q4.
Bill Jahangiri: Thank you.
Operator: Thank you. And our next question coming from the line of Li Watsek with Cantor. Your line is open.
Li Watsek: Hey, guys. Thanks for taking our questions. And Shawn, I want to add my congrats as well. So, I guess for AFM13 cohort 1 and 2, wondering if you can comment on, I guess, how many of these 12 patients is still on study, and what are you seeing in terms of durability. And then, also curious for the patients that achieve partial response, wondering if you can comment on the kinetics of the response and trends you're seeing in terms of deepening response.
Shawn Leland: Hey, Li, thanks for the welcome and congrats. Andreas, do you want to follow-up on her questions?
Andreas Harstrick: Yeah. So, I think for duration of response or our general duration question, the follow-up is just too short. We initially had a staggered enrollment. Obviously, the two patients with progressive disease who did not respond have left the study, but the majority of patients is still on treatment. As we said, for example, three of the four patients with a PR are still on treatment. The complete responses that we have reported, the six complete responses, they were all complete response after the first cycle. So, there is, obviously, technically no way to see further kinetics. But when we refer or when we take into account our experience that we had at MD Anderson, roughly one-third of the patients that ultimately achieved a complete response were partial responders after cycle one and then with additional cycles got into a complete response. So, we will have to wait until we have completed the treatment of these three additional patients to be able to really comment on the response kinetics. Again, the six patients that we are reporting right now is complete response or were complete responders after the first cycle.
Li Watsek: Okay, great. And I have a follow-up question in terms of the screening failure rate. I wonder if you can just comment on what you're seeing now. It seems like you made pretty nice enrollment progress for cohorts 3 and 4. Was that more driven by maybe more sites or initial data or maybe a combination of factors? And is this sort of a good run rate of enrollment pace that we should be thinking about as you move into the randomized portion?
Andreas Harstrick: Yeah. We -- as I said, we are really happy with enrollment in cohorts 3 and 4, but this is something that you often see in trials that initially you have to do some training of the sites. And then, we also had a couple of patients who just dropped out because of infectious complications. Now, I think sites have the right feeling for the right patients. We also have more sites. I'm very encouraged by the enrollment. Whenever you move from a single-site study, especially if it's an academic center like MD Anderson, there are always some concerns whether you can reproduce this in the real-world setting, if you will. But now with 10 sites actively enrolling patients and still producing these outstanding data, I think, it's indicating that this is a treatment that can really be given across the country and can reach many patients in need, because basically every site that has some experience with lymphoma treatment can administer this type of treatment.
Operator: Thank you. And our next question coming from the line of Yanan Zhu with Wells Fargo (NYSE:WFC) Securities. Your line is open.
Unidentified Analyst: Hi. Thanks for taking our question, and congrats, Shawn. And this is [Kuan] (ph) on for Yanan. So, my question is on acimtamig. You mentioned that the response rate is like consistent across cohorts 1 and 2. I wonder if there is a dose response on the CR rate? Thank you.
Shawn Leland: Kuan, thanks for the welcome and congrats. Andreas, do you want to speak to the potential dose response with acimtamig?
Andreas Harstrick: Yeah. As we already said, currently, we have not seen a difference in responses between cohorts 1 and 2. So, no difference in 200 milligrams or 300 milligrams of acimtamig. We also have not seen any difference in toxicity. Again, with longer follow-up, we will have to evaluate whether there is a difference in terms of duration of responses. Now, with cohorts 3 and 4, we ask the second important question, which is whether a higher dose of the AlloNK cell will make a difference, but here we have to wait until the data a little bit mature. But again in terms of response rates, no difference between 200 milligrams and 300 milligrams.
Unidentified Analyst: Got it. And that include the CR rate, right?
Andreas Harstrick: Yeah.
Unidentified Analyst: Okay, great. Thank you. And on AFM24, can you remind us the bar on PFS? And any updated data on PFS you can share with us on both wildtype and mutant? Thank you.
Shawn Leland: Yeah. Andreas, do you want to speak to the question?
Andreas Harstrick: Yeah. So, again, for the wildtype, we have the data that we disclosed at our last earnings call where the PFS was 5.9 months. We have not updated PFS for the additionally enrolled patients. This is something that probably will be available Q1 2025. We will have response data for the expanded EGFR wildtype cohort in Q4 of this year. As we reported for the EGFR mutant cohort today, we still have roughly 50% of [six] (ph) patients that are response-evaluable on treatment with a meaningful follow-up of seven months. So, we don't have the mature PFS yet. Again, these responses that we see, and this is exactly the same with EGFR wildtype and EGFR mutant cohorts, they seem to be durable. As we said, all four responders have been on treatment for at least seven months. When we reported EGFR wildtype cohort, again, the responses were lasting seven, eight and nine months. And still some of these patients were ongoing at eight and nine months. But we'll need for both cohorts a little bit more maturation of the data to have a final PFS number. As a reference, again, single-agent chemotherapy or even chemotherapy in combination with VEGF inhibiting agent like CYRAMZA usually produces PFS data of 4 or 4.5 months. So, seeing roughly half of the patients still on trial at seven months is, for us, highly encouraging, as the data in the EGFR wildtype cohort where we have close to six months of PFS.
Unidentified Analyst: Got it. That's super helpful. Thank you.
Operator: Thank you. And our next question coming from the line of Brad Canino with Stifel. Your line is open.
Brad Canino: Hi, and thank you. Shawn, nice to hear you on the call. I do have a question for you. I think when I look at your past history, a majority of your experience has been the development of drugs with distinct monotherapy activity. And I think here you've got AFM24, the activity signal derived from single-arm data, uncontrolled in combination with the drug that is known to have some limited salvage activity. So, it would be great if you can walk me through your diligence process and how you vetted the potential contribution of the parts or perhaps the right word is synergy from AFM24?
Shawn Leland: Yeah. Thanks, Brad, and great to hear from you. I mean, I think overall looking across kind of the portfolio of Affimed products, I mean, I think what's quite encouraging is the fact that there's great validation of the platform technology across not only solid tumors in terms of what we've seen with AFM24 in combination with anti PD-1, but also in the hematologic malignancy space as it relates to what we've seen with the acimtamig, and then also with what we've recently been seeing with AFM28. I mean, I think that there is clear signs that there's monotherapy activity that's been seen with these products, but I also believe that there is perhaps greater potential with the combinations. So, that is really kind of what was seen in my due diligence. I think a lot of my due diligence was also looking at where this data stacks up against competitors, Brad. And, I mean, kind of taking them kind of, like, one step at a time here, right? I mean you look at the acimtamig program, seeing a 83% response rate with a 50% CR rate, and what is arguably a much more heavily pretreated population than what's in the ADCETRIS label, for example, and then also what's in either the Opdivo or Nivolumab labels, I mean, this is highly encouraging. I mean, this is something that, from my perspective, could be a best option for patients with Hodgkin's lymphoma. I mean, this is a very heavily pretreated patient population. So, I'd also look at this from the perspective of being able to address unmet medical needs. And yes, historically, I've focused in kind of the precision oncology monotherapy space, but I think more and more as we see the field of oncology move, a lot of that movement is towards that of combinations. I mean, I think with AFM24, I mean, I think as Andreas has highlighted, there's not really any great options for these patients in the settings where we are studying them. I mean, typically, you do not see for the EGFR mutated cohort, which is what we kind of focused on as it relates to the update today. I mean, there's not really anything out there for those patients. I mean, you're basically talking in a single-agent chemotherapy or going on to a clinical trial, which is kind of the NCCN recommendation post EGFR TKI and post products like, amivantamab and lazertinib. So, I mean, I think the data is highly encouraging and it's also quite encouraging since we typically don't see any monotherapy activity of anti PD-1 in this population. This idea of being able to combine two therapies, one that targets the innate immune system and one that targets the adaptive immune system, there seems to be a synergistic effect and there seems to be really nice benefit in these patients who really have no other therapeutic options.
Brad Canino: Appreciate all the commentary around that. Thank you.
Operator: Thank you. And our next question coming from the line of Swayampakula Ramakanth with H.C. Wainwright. Your line is open.
Swayampakula Ramakanth: Thank you. This is RK from H.C. Wainwright. Welcome aboard, Shawn. Most of my questions have been answered. I just have a quick question on the AFM24 program. Now that we have data from both the wildtype and the mutant EGFR patient cohorts, how do you plan to take these studies forward? And is there a plan to expand these cohorts initially to strengthen the data before going into the next level of clinical development? That's it from me. Thanks.
Shawn Leland: So, thanks for the question and as well as for the welcome. Andreas, do you want to speak to his question?
Andreas Harstrick: Yeah. So, I think, these decisions, very good question, will be data driven. What we have done, especially for EGFR wildtype, we have already expanded. As you know, we initially reported 17 patients. We have now a cohort that is basically fully enrolled with a target patient population of 40 evaluable patients. So, this will give us a significantly broader data set. Again, we expect to have response data by year-end and then PFS data early 2025. And then, we will have to make strategic decisions how to proceed. Again, with the PFS that we are currently seeing also with the tail with the duration of the responses, we believe that we could beat the standard of care in this area, which would be our docetaxel plus/minus ramucirumab. EGFR mutant is even a more, I would say, deserted field once patients do not respond anymore to TKIs and platinum-based chemotherapy, even palliative care is considered. So, based on the data and if the data mature a little bit more, we will have all these discussions. We also start interactions with the regulatory agencies and then really form also best way to potential market approval.
Swayampakula Ramakanth: Thanks, Andreas. Thank you very much for taking the question.
Operator: Thank you. And I'm showing no further questions in the queue at this time. And ladies and gentlemen, that does conclude our conference for today. Thank you all for participating, and you may now disconnect.
Shawn Leland: Thank you.
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