Affimed N.V.

Good day, everyone, and welcome to AFI Med's first quarter 2024 earnings and corporate update call. At this time, all participants are in a listen-only mode. Later, we will conduct a question and answer session, and instructions will be given at that time. As a reminder, today's conference call is being recorded. I would like to introduce your host for today's call, Alex Vedakis, Head of Investor Relations at AFI Med. Please go ahead.

Thank you, Michelle, and thank you all for joining us today for our first quarter 2024 update call. Before we begin, I'd like to remind everyone that we issued the relevant press release and presentation on our website today, which you can find in the investor relations section. On the call today, we have members of our management team, including Andreas Harstrick, our chief medical officer and acting chief executive officer, Wolfgang Fischer, our chief operating officer, Denise Mueller, our Chief Business Officer, and Harry Welton, our Consulting Chief Financial Officer. Our financials today will be presented by our Vice President of Finance, Michael Wolff. 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 future 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 and our filings with the SEC, and those identified under the section entitled forward-looking statements and the press release that we issued today and filed with the SEC. With that, I'll turn the call over to Andreas. Andreas?

Yeah, thank you, Alex, and good day, everyone, and thank you for joining us today for our first quarter 2024 earnings call. I'm excited to share with you today clinical data on all three of our clinical programs that as we believe are validating our approach of using the innate immune system as an additional tool to fight cancer. When we announced the strategic reorganization of AFIMED and our focus on the advancement of our clinical assets in January, We guided that our goal would be to generate meaningful data for all three programs in the first half of the year. I'm proud to say and thankful to all of my coworkers at AFIMED and to all our clinical investigators that today we can deliver on this guidance. As shown on slide three, we now have clinical validation for all three assets. For AFM24, we are advancing the combination study with atezolizumab in treatment refractory patients with non-small cell lung cancer, both in the EGFR wild type and in the EGFR mutant subgroups. Data that we shared at ASCO demonstrate durable responses in patients with EGFR wild type tumors with three or four responses ongoing now for over seven months. We also see meaningful and confirmed tumor responses in the EGFR mutant subgroup, a tumor type that is generally considered unresponsive to immunotherapy. We can also share exciting data for our clinical LUMINISE trial of a symptomic in combination with LONK cells in patients with refractory Hodgkin's lymphoma. Seven patients have had their CT scans meanwhile assessed by blinded independent read, which will be the primary endpoint of the study as agreed upon with FDA. In these patients, we see objective responses in six out of seven patients. for an overall response rate of 85.7%. Importantly, this includes four patients with a complete remission. Finally, AFM28, our CD123 targeting ICE for the treatment of refractory AML has shown remarkable clinical activity. At dose level five of our single agent dose escalation study, we have observed one complete response and five patients with stable disease. At dose level six, we see two patients with a complete response and a CRI respectively, and three patients with stable disease. Importantly, the complete response from dose level five is now ongoing and stable for more than five months, and five of the six patients at dose level six are continuing on treatment with a possibility for further deepening of their responses. Also importantly, no dose limiting toxicities were observed in dose level five and six, thereby establishing a safe and effective regimen for further development. Let us look at the data in some more detail. Today, I will start with a symptomic. As a reminder on slide five, you see the trial design as agreed upon with FDA. We now have completed enrollments into cohorts one and two and are actively recruiting cohorts three and four. We admit that there is still a slight delay in recruitment compared to our initial expectations as discussed on our last earnings call. This is mainly due to a higher rate of patient dropout during the screening period. However, with additional sites now active and more experience with the protocol at the site level, we expect to see further improvement in patient recruitment and a reduction in the dropout rate. In terms of safety, shown on slide six, The adverse event profile is in line with our previous experience with asymptomic and the combination of asymptomic and allogeneic NK cells, respectively. It is important to note that in the LUMINISE 203 study, we did not use steroids as part of the premedication for asymptomic, and therefore, we were expecting a slightly higher rate of infusion-related reactions compared to some studies with a symptomatic in which steroid premedication was routinely used. Four of seven patients developed a grade one or two infusion-related reaction slash CRS event. One of these four patients had a short-lasting grade three CRS, as assessed by the investigator, which manifested mainly by high fever and a decrease in blood pressure However, the patient responded readily to standard of care treatment. Importantly, in this patient, shortly after this event, there was also an acute CMV infection diagnosed, and thus the relative contribution of the infusion of a symptomatic versus acute CMV infection to the overall symptoms is not clear. Importantly, there were no treatment discontinuations due to side effects of asymptomic or LONK. Also, there were no instances of bleeding, ICANNs, or graft versus host disease. As a clinical activity of the combination is, I think, remarkable as shown on slide seven. Six of seven patients showed an objective response by independent read, including four patients with a complete remission. These data are directly comparable with the data that were reported by MD Anderson Cancer Center for a symptomic in combination with fresh pre-complexed NK cells, and thus indicate that co-administration of an ICE with allogeneic NK cells is active, that no pre-complexing is needed, and that cryopreserved NK cells seem to be comparable to fresh NK cells in terms of anti-tumor activity. Also, these results demonstrate that data from the single site study at MD Anderson are reproducible in a multicenter setting as these seven patients were enrolled by four different institutions. Slide eight shows the patient's characteristics underscoring that these patients are heavily pretreated with a median of four lines of previous therapy. All patients had failed combination chemotherapy, PD-1 targeting therapy, and brentuximab. In addition, five of seven patients had also failed after autologous stem cell transplant. On slide nine, you see an example of a patient with multiple manifestations of his refractory Hodgkin's lymphoma, including axillary lymph nodes, supraclavicular lymph nodes, spleen, and inguinal lymph nodes. The patient had failed all standard of care options, including stem cell transplant, and presented with B symptoms, which clinically is a very unfavorable prognostic factor. As you can see, all tumor manifestations resolved after only one cycle of therapy. Let's move on to AFM24. Since we presented the data in detail during our ASCO presentation, I will be brief here. As shown on slide 11, the combination of AFM24 and etizolizumab has meaningful activity in patients with heavily pre-treated EGFRY-type non-small cell lung cancer. In 15 evaluable patients, there were four objective responses and eight patients with stable disease. Of note, all patients had failed combination chemotherapy and PD-1 targeting therapy. All responders were documented progressive on previous anti-PD-1 treatment. Importantly, the responses and the tumor control induced by AFM24 atizolizumab appear to be durable, as shown on slide 12, where you see the long-term follow-up data. The progression-free survival for the whole study population is 5.9 months, which compares favorable to the 4.5 months, which is usually achieved in these patients with standard of care treatment. Even more encouraging is the fact that three of the four remissions are still ongoing, now at more than seven, more than eight, and more than nine months, respectively. It appears very unlikely that these data can be explained by atezolizumab activity alone. Even though there are occasional responses to PD-1 re-challenge after intervening chemotherapy, PFS data in these patients have been very short. Even in PD-1 non-pretreated patients, in platinum refractory non-small cell lung cancer, atezolizumab has shown a progression-free survival interval of only 2.8 months. Our recent results in patients with heavily pretreated EGFR mutant non-small cell lung cancer, as shown on slide 13, support the activity of the AFM24-Atezolizumab combination. In 13 patients that are response-evaluable, four responses and six patients with stable disease were achieved. Compared to the data that we reported at ASCO, meanwhile, all objective responses have been confirmed by follow-up scans, and all responses are ongoing. This is remarkable as EGFR mutant non-small cell lung cancer is in general regarded as unresponsive to immunotherapy. Slide 14 shows the market opportunity for drugs that are targeting refractory non-small cell lung cancer. In the seven major markets, there are 175,000 patients with EGFR-Y type non-small cell lung cancer, and roughly 35,000 patients with EGFR mutant non-small cell lung cancer annually who fail standard of care therapy and will need additional treatment options. Current treatment options for these patients are unsatisfactory, with PFS durations around 4 to 4.5 months. Also, many salvage regimens include chemotherapy, that is often difficult to tolerate for these heavily pretreated patients. The combination of AFM24 plus PD-1 could provide a chemotherapy-free alternative with meaningful activity and significantly better tolerability for these patients. Finally, let's review the most recent data of AFM28 our CD123 targeting ICE for the treatment of acute myeloid leukemia as shown on slide 16. Here we have escalated the dose through six cohorts up to 300 milligrams weekly. I think this study is also a good example of the ability of our organization to execute clinical studies. The first patient in this program was treated in March 2023 And the whole dose escalation trial over six cohorts was executed in only 15 months. The safety profile is shown on slide 16. For dose levels five and six, we did not see any dose-limiting toxicities. The most frequent side effects were infusion-related reactions, mainly of low grade. Only three patients had a grade two infusion-related reaction responding in all cases to symptomatic treatment, and there were no grade 3 or higher IRRs. One patient experienced a short-lasting self-limiting CRS of grade 1. Infections are characteristic manifestations of acute leukemia and were seen in half of the patients. However, none of the infections was considered treatment-related by the investigators. In addition, we observed meaningful target interaction at doses of 200 milligrams and above with near complete saturation of CD123 binding sites on the tumors and occupation levels of CD16A on the NK cells that in preclinical experiments result in potent NK cell activation. The clinical activity is displayed on slide 17. In dose level five, we saw one complete response and five patients with stable disease. All patients were heavily pretreated. Of note, the complete remission is still ongoing after more than five months. In dose level six, we saw two patients with a complete response and a CRI respectively, and three patients with stable disease. Five patients from dose level six remain on treatment with additional cycles, and thus was the option to deepen their responses. I think these results are remarkable. Most of these patients with advanced AML have very low numbers of own NK cells when they start treatment. So it appears that AML could be very sensitive to NK cell mediated killing if already low numbers of endogenous NK cells when directed to the leukemia cells by AFM28 can produce complete responses. These data taken together with impressive activities that we have seen with a combination of a symptomatic and allogeneic NK cells in Hodgkin lymphoma, support our strategic intent to pursue further development of AFM28 in association with a cryopreserved allogeneic NK cell product. With this, we would, again address 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. Many of these patients are elderly and show frequent comorbidities, thus limiting the use of aggressive chemotherapy. Immunotherapy has not been successful so far in AML. A treatment approach based on the activation of the innate immune system could therefore be an important additional strategy for the treatment of these patients. With this, I will close the overview of our clinical programs and hand over to Michael Wolf for a review of our financial data. Michael, please.