Thank you for standing by, and welcome to the Affimed Third Quarter 2021 financial results and corporate update conference call. At this time, all participants are on listen-only mode. After the speaker's presentation, there will be a question-and-answer session. [Operator Instructions]. As a reminder, today's program is recorded.

I would now like to introduce your host for today's program, Alex Fudukidis, Head of Investor Relations. Please go ahead, sir..

All right. Thank you, Jonathan. And thank you all for joining us today for our Third Quarter 2021 results and operational update call.

Before we begin, I would like to remind everyone that we issued the relevant press release earlier today, and that it can be found on the Investor Relations section of our website on the call today, we have the following members of our management team, doctors Adi Hoess Chief Executive Officer, Andreas Harstrick, our Chief Medical Officer, Arndt Schottelius, Our Chief Scientific Officer, Wolfgang Fischer, Chief Operating Officer.

Ms. Denise Miller, our Chief Business Officer, and Angus Smith, our Chief Financial Officer. The whole team will be available for the Q&A sessions. Before we start, I will quickly go through the 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 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, and the press release that we issued today and filed with the SEC.

With that, I'll turn the call over to Adi. Adi..

Thank you Alex, and good morning everyone. Thanks indeed for joining our Third Quarter updates call. I'm very pleased with continued progress towards our goal of bringing new and innovative life-saving medication to cancer patients who need them. Our pipeline possessions has for several potential value breaking milestones through the end of 2022.

Today, in addition to providing an update on our leading programs where we'll spend a little bit of time to introduce you to AFM 28. Our most advanced pre -clinical [Indiscernible] which is expected to enter the clinic in 2022. On slide 3 of the presentation that we made available to accompany our call today.

We summarize optimist strategy for developing our index selling digit. We introduced our 3-pronged development strategy to you about a year ago. As we said to you, then we believe this strategy allows us to explore different development approaches, thereby increasing the probability of success for each of our molecule.

What we have learned to date about the safety of our molecules is indeed supporting not just mono-therapy, but also combination approaches. The first approach where the patient's own innate immune system in is well functional in the involves developing our [Indiscernible] molecules as monotherapy.

Our combination therapy approach involves the 3 novel therapeutic combination, including combinations with NK cell therapy and other I-O to I-O therapies such as checkpoints inhibitors. In the case of -- in case of combinations, the combines those [Indiscernible] car light intake therapeutic that seek out and destroy tumors.

An example of that is our investigator-sponsored clinical trials at MD Anderson Cancer Center. On slide 4, we are showing where we are with our leading in Innate Cell Engagers.

From 13 and 8, from 24, and the recently added AFM 28 in a nut shell, all three of these Innate Cell Engagers binds to CD 16A on natural killer cells and macro pain with higher affinity and also binds on specific targets on cancer cell to bring the innate immune system to fight against cancer.

This slide shows our AFM13 Innate Cell Engagers target CD30 -positive lymphoma, AFM24, key trader far expressing solid tumor and AFM28 on years candidate CD123 -positive AML in the pension.

We are embarking on a broad development strategy for each of our molecule, which we believe we will be the basis for continuous data flow from our pipeline over the next several quarters. Since we introduced into our 3-pronged strategy, we've also made a lot of progress to support our thing.

We have published clinically and pre -clinically data that make us quit confident about the path that we have set for our company. Our goal in all of these efforts at Optimal is to bring innovative therapies to cancer patients who are often out of these options when it comes to managing their disease.

These are very sick patients who are frequently see their disease return up to multiple lines of treatment. Very proud to have been able to offer these [Indiscernible] (ph) and frequently, without hope, patients, another opportunity to fight their disease.

And as we have shown, for example, with [Indiscernible] 13 and in particular, in combination with natural colorful. With that introduction, let me give you a quick update on our progress. Jumping now to slide 6.

This shows that naps of where we are with [Indiscernible] Our registration directed [Indiscernible] compared to mono-therapy in relapsed or refractory peripheral T-cell lymphoma is on track to complete enrollment in the first-half of 2022. And we expect to product guidance about timing for data as we get closer to the completion of enrollment.

We're also very pleased to share with you that investigator sponsored clinical trial at MD Anderson Cancer Center evaluating cord blood-derived Natural Killer cells pre -complex with 8 and 13 is going very well.

As of October 31, a total of 18 patients have now been enrolled in the study including 12 patients at the highest dose, where we use 10 to the 8 in case of per kilogram on patient weight. We can confirm that no dose limiting toxicities have been observed and we continue to be encouraged by the response rate.

To date, our key learning are that the dosing regime is well tolerated and can drive for robust anti-tumor responses in heavily pre -treated patients.

Our goal is to continue to gather over state and safety and efficacy, and according to the MDA MD Anderson have submitted a protocol amendment to allow for an expansion of this study to treat up to 40 patients at the highest dose, now including lymphoma patients and the just tested positive and non-Hodgkin lymphoma patients.

Finally, we plan to present updated data from the study at the company sponsored event in mid-December and expect to provide additional details on the date and time for this event in the coming week.

We're also very excited about our progress with AFM24 where we believe the execution of our 3-pronged strategy will allow for a continuous state of flow of data over the next -- over the course of the next several quantum. To advance our Chief Medical Officer will now tell you more about where we are with AFM24, Andreas..

Yes, thank you, Adi, and good morning, good afternoon to all of you. It's my pleasure and my privilege to give you an overview of our development program with AFM24 and to review some of the recent progresses that we have made in this program. If you move to slide 8, this slide gives you an outline of the development strategy for AFM24.

As you'll see, it's a very comprehensive, very broad development approach. We expect to investigate AFM24 as a mono-therapy, and in combinations with either PD - L1 inhibitor atezolizumab or with auto logos, NK cells and a total of 7 different indications across 9 expansion cohorts.

This broad approach is intended to deliver the highest probability of success for AFM24, both as single agent and as combination partner. On slide 9, we demonstrate the process that we used to select indications and to maximize profitability of success.

The selection of indications for each studies was based on a very slow and very comprehensive analysis that used data of more than 10,000 patients across 144 tumor sub-types.

And these were initially ranked based on 20 criteria, but included, but are not limited to factors like EGF receptor expression, involvement and functional cyanate immune system in the tumor microenvironment. But also looking at unmet medical need and potential passes to market.

If we can move to Slide 10, we show you the general concept that applies to all of our studies. All studies are based, as I said on a selection of indications that individual situation we believe have the best chance of therapeutic success. The individual cohorts in each of these studies follow an optimized Simon 2-stage design.

This design provides us with an opportunity to make gated investment decisions. In the first step each cohort will recruit 12 to 18 patients after which we have a pre -planned interim analysis. This interim analysis is associated with pre -defined success thresholds.

In the case that individual success thresholds are met, we will recruit up to 40 patients in each cohort, and we believe that this number of patients will give us summit data to start conversations with regulatory agencies about registration strategies.

Furthermore, since these are open-label studies, we will have the opportunity for interim data readouts. With that said let me update you on the development of AFM24 in our mono-therapy study, which is shown on slide 11. As you're all aware, the initial part is a dose escalations part, in order to define the recommended phase 2 dose.

It is important to reiterate that the goal of the dose escalation part was to identify the pharmacologically active and safe dose of AFM24 as fast as possible. Therefore, in the dose escalation part, there was no selection of patients with tumors that are more likely to respond to single agent, as defined by our indication selection process.

Slide 12 shows you're at the recruitment status so far. Up to now we have recruited 29 patients across 6 dose cohorts. As you can see, the study population covers a wide range of tumor indications with colorectal cancer harboring either Ross or Ross mutations, being the most frequent tumor type.

Also important to note that all of these patients were heavily pretreated with immediate number of previous therapies of 4 and a range of 2 to 8 previous therapies. All patients have exhausted all available treatment options for as they're given tumors. On Slide 13, we provide a summary of the patients that were treated at the 480 milligram cohort.

Off Note, 4 out of 6 patients are still receiving therapy with AFM24, as they are deriving clinical benefit according to the assessment of the treating physicians. 2 patients have shown stable disease beyond 3 months and continue treatment.

A specific note, patient 5 while classified with progressive disease has experienced a meaningful clinical benefit and also continues on treatment. We plan to submit detailed data from the dose escalations for a presentation at a medical conference in the first half of 2022.

Moving on, we are pleased to announce that we have determined that 480 milligrams is a safe and pharmacodynamically active dose and will be our recommended phase 2 dose for weekly administration.

As outlined in slide 14, this decision is based on a comprehensive review of safety, pharmacokinetic exposure and pharmacodynamic data, including CD16 A receptor occupancy on peripheral and K cells.

As supportive pharmacodynamic data, we have also measure the [Indiscernible] of serum cytokines and markers of immune cell activation, which exhibit continuous activation of NK cells at doses of greater than 160 milligrams. From a safety perspective, no dose limiting toxicities were observed at either 320 or 480 milligrams.

In the next two slides, we seal the data on the pharmacokinetic intor receptor occupancy that has reported the recommended phase 2 dose decision. Slide 15, you'll see the PK profiles of all dose cohorts.

As shown on the left side, we observed a proportionality of dose and exposure at doses of 320 milligrams and 480 milligrams, which indicates that we achieved saturation of target mediated elimination by EGFR. Meaning that EGFR receptors at these doses are likely saturated.

In the graph of the right side, you also see that the track levels that we are reaching with 320 milligrams and 480 milligrams shown in green and blue dots are comparable to Cetuximab trough levels at the market at Cetuximab dose indicated as a gray faded area.

If you move to Slide 16, we review here as the data that we have obtained was CD-16 receptor occupancy. And I will take a minute to walk you through the slide. On the last graphs you'll see the measured CD-16A receptor. occupancy on circulating and K-cell s.

As you can see, that we initially see an increase in CD16 A occupancy was increasing doses, which Platos at 480 milligrams, indicating a saturation of CD 16 A of proliferate. Now, the important question is, how does this translate into the tumor? And how was this correlated to activity? On the right you'll see 2 curves from our in vitro studies.

The blue curve is tumor cell killing by NK cells in the presence of AFM24. The red curve is CD16a receptor occupation. As you can see, maximum tumor cell killing is achieved with dose ranges that are associated with relatively modest CD16a occupancy.

It is important to note though that when we speak about relative receptor binding, let's say of 10%, this does not mean that we have only activated 10% of NK cells. Every NK cell has bound a AFM24, but on the individual cell level there is a 10% occupation of available receptness which already translates into maximum cytotoxicity.

Now, the vertical line here indicates a drug level of AFM24, we expect in the tumor at a dose of 480 milligrams. For this calculation, we have taken a very conservative assumption, which is at AFM 24 concentrations in tumor tissue will be 200 fold lower than in circulating blood.

But as you can see that even under these very conservative assumptions, 480 milligrams result in the CD16 A occupancy into the tumor that is sufficient for maximum NK cell activation. In summary as stated on slide 17, our decision for 400 milligram as a recommended phase 2 doses based on the good safety profile.

And so PK and PD data that I just showed. As next steps, we plan to open expansion cohorts at 480 milligrams to explore anti-tumor activity in three selected indications.

In parallel, we also plan to continue dose escalation of AFM24 to 720 milligram just currently open for patient enrollment to gather additional safety data and provides the basis for alternatives, scheduling, like a once every 2 or once every 3 application of AFM24.

If we now turn to the 2 combination studies, mainly the combination with NK and auto logos NK cell, AFM24 103, and to combination study with atezolizumab AFM 24 102.

For both of these trials, the starting dose of AFM24 will be a 160 milligrams, followed by dose escalation steps, for which we will assess safety and identify a recommended phase 2 dose for the combination.

These recommended phase 2 doses will then be used in the dose expansion phases, which as I described, will follow assignment 2 stage design in 5 of the 6 cohorts, with [Indiscernible] analysis up to 12 to 18 patients and the ability to enroll up to 40 patients.

On Slide 18, you'll see the design of 1 or 2 study where we combine AFM24 with atezolizumab. In this trial, we will focus on non-small cell lung cancer, gastric cancer, and hepatobiliary pancreatic cancer. All areas of very significant unmet medical need.

The cohorts in non-small cell lung cancer and gastric cancer follows a described Simon 2 stage design. The third cohort that can include hepatocellular cancer, biliary tract cancer, and pancreatic cancer, is designed as a signal identifying basket cohort with descriptive statistics.

If we move to Slide 18 here we saw of the design of our study 24,103, a combination of AFM24 with adoptive NK cell transfer. This study will focus on non-small cell lung cancer, colorectal cancer, and head and neck cancer.

We will loose this innovative approach in these indications where patients endogenous NK cell numbers are dysfunctional or only existence of efficient numbers has a good opportunity to show activity.

In contrast to the 101 study, where we also evaluate CRC, but require previous treatment with EGFR antibodies and thus we'll most likely exclusively recruit CRC patients with key RAS wild-type. The CRC code in 103 will focus mainly on patients with key RAS mutations.

Finally, on AFM24 you may have seen the presentation of the most recent triple meeting where we showed that AFM24 enhances cycotoxicity against EGFR -positive tumor cells when combined with SNK01 the auto logos and Keisar product.

The additional for AFM24 total over SNK01 cells improved self-healing when compared to NK cell to known in EGFR positive tumor cell lysis, regardless of EGFR mutational status.

To summarize on slide 19, the status of CAF from 24 program, we are very excited that we can now embark on a broad development program in several indications with significant unmet medical need. This study as shown will generate a continuous flow of data in 2022 and beyond.

With that, I will turn the call over to my colleague, Arndt Schottelius, who will present our novel fully-owned ICE AFM 28. Arndt, please..

Thank you, Andreas. And also for me, good morning. Good day, everybody. Warm welcome to the call. I'm really excited to introduce AFM 28 to all of you, which is our newest edition for our portfolio.

As shown on Slide 21, we recently announced our newest in 8 cell engage or AFM 28, which is designed to bind CD-123 and establish targets and myeloid malignancies.

Which shows CD-123 as it is almost geniuniversally expressed on leukemic blasts, and leukemic cells in patients with AML, both adds diagnosis and Ed relapse, and independently of cytogenetic risk. AFM28 is being developed for the treatment of patients with acute myeloid leukemia.

We believe that AFM28 would be the key to novel treatment approaches that can fulfill several unmet needs. I would like to spend a few minutes to explain there some layout, why we're so excited about adding AFM28 to the arsenal against leukemia.

AML is the most common form of adult acute leukemia, more than 40,000 patients are diagnosed with this disease every year in the seven major markets, the outcomes have remained very poor and treatment options are generally limited, particularly for relapsed or refractory disease.

As shown on side 22 in AML, most patients become refractory to standard induction treatment or relapse within 1 year. Only 1 of 3 patients is alive after 1 year once they become relapsed or refractory. After 5 years, it is only 1 out of 10 patients.

It is obvious that new drugs are needed that reduced the high rates of relapsed or prolong the time to relapse while using deeper responses, and by eradicating measurable residual disease or MRD.

In addition, for patients who have relapsed or are refractory to standard treatment, alternative options to reduce readmissions of a long-lasting are urgently needed. These all needs to be achieved for patient population that is elderly. Note that over 80% of patients are over 60 years old.

And can often not tolerate treatments associated with toxicity. So these new approaches not only need to be more effective, they also need to be safer. Recent data have demonstrated that natural killer cell based innate immunotherapy is emerging as a promising treatment option in AML.

Based on the demonstrated susceptibility of leukemic glass for NK cell killing and clinical activity of [Indiscernible] NK cell therapy and relapsed refractory disease. Also, these treatments are remarkably well tolerated. Yet these approaches rely on the cells natural ability to recognize leukemic cells.

So these cells are not specifically targeted against the tumor. Immune evasion from NK cell killing is a well-known phenomenon and escape of leukemic stem cells and AML has been described.

To effectively deplete leukemic cells, including leukemic stem cells, a targeted approach in addition to natural cytotoxicity has the potential to induce more frequent and deeper responses. We believe these statements are also supported by the data that we have generated with AFM13 in combination with NK cell.

We designed AFM28 to be differentiated versus available therapy, and to bring a truly novel approach to the treatment of AML. As we've shown on Slide 23, AFM28 binds with highest synergy to both CD123 and CD16A and no such molecule currently exists to our knowledge.

It thereby strongly activate NK cells, inducing ADCC and through binding to CD123 causes depletion of leukemic cells and leukemic stem cells. We will be presenting preclinical data for AFM28 at ASH and plan to submit an IND application in the first half of 2022 and to start a clinical study in the second half for 2022.

With that, I will hand the call over to Angus to review the financials.

Angus?.

Thank you, Arndt. AffiMed 's consolidated financial statements have been prepared in accordance with IFRS, as issued by the International Accounting Standards Board or IASB. The consolidated financial statements are presented in euros, which is the company's functional and presentation currency.

Therefore, all financial numbers that I will present in this call unless otherwise noted, we will be in euros.

We ended the Third Quarter of 2021, but cash and cash equivalents of a EUR198.7 million compared to a EUR146.9 million on December 31st 2020, based on our current operating plans and assumptions, we anticipate that our cash and cash equivalents will support operations into the second half of 2023, net cash used in operating activities for the quarter ended September 30th, 2021 was EUR25.6 million compared to EUR3.6 million in the third quarter of 2020.

Total revenue for the Third Quarter ended September 30th, 2021 was 8.7 million compared to 25 million for the quarter ended September 30th, 2020. Revenue for the third quarter of 2021, mainly comprised of collaboration revenue from Genentech and ROI event.

Research and development expenses for the Third Quarter of 2021 was EUR 20.6 million compared to EUR 10.1 million for the Third Quarter of 2020.

The increase in R&D expenses compared to the same period last year for driven primarily by increased expenses for AFM24, including costs for the production of clinical trial material, and increase in costs associated with other early stage programs and infrastructure, and an increase in share-based payment expense.

General and administrative expenses for the Third Quarter of 2021 or EUR6.8 million compared to EUR 3.5 million in the quarter ended September 30th 2020. The increase relates largely to higher personnel expenses, higher premiums for insurance, higher consulting expenses, and increased share-based payment.

Net finance income for the quarter ended September 30, 2021 was EUR1.5 million compared to net finance loss of EUR3.1 million in the quarter ended September 30, 2020. Net Finance Income loss is largely due to foreign exchange gains or losses related to assets denominated in U.S. dollars as a result of currency fluctuations between the U.S.

dollar and the Euro. Net loss for the quarter ended September 30, 2021 was EUR17.1 million or EUR0.14 cents for common share compared with a net loss of EUR6 million or EUR0.07 per common share for the quarter ended September 30, 2020. The weighted number of common shares outstanding for the quarter ended September 30, 2021 was EUR119.8 million.

With that I will turn the call back to Adi for closing remarks, Adi..

For our Global Head and Investor event in December where we plan to provide a data update on our ongoing trials in combination with Natural killer cells. In addition play to monotherapy in peripheral T-cell lymphoma, we expect a complete enrollment in our registration directed study in the first half of next year.

With broadly explained understanding with AFM24 and for monotherapy we are now planning to open the expansion cohort before the end of this year. We submitted abstract with data from the dose escalation for presentation at a medical conference in the first half of 2022.

And then as we move forward with the expansion cohorts, we record initial data in 2022. We have set up 2 additional studies for AFM24 in combinations, either with nitric killer cells, or we're [Indiscernible] anti - PD-L1 atezolizumab.

We are expecting to complete the first dose escalation cohort in each study during the first - half of 2022, start with the dose cohort expansion, if safety is favorable and thereby also be able to provide updates as we progress. For AFM28, a very new candidate that we carefully selected in order to address the high medical need.

After now the ASH data update, our next milestone, are the planned IND submission in the first half of 2022. And subsequently, the initiation of clinical studies. We're planning again, as explained before, to do this in monotherapy. And also combinations in particular -- in combination with natural killer cell.

We're preparing the company to meet need opportunities and look forward to bringing innovative medicines to patients that need them. Now on behalf of the entire team, I would like to once again express my gratitude to everybody who is contributing to these efforts. We are now ready to take any questions that you may have. Operator..

[Operator Instructions]. Our first question comes from the line of Daina Graybosch from SVB Leerink. Your question, please..

Hi. Thank you for the questions. Just looking at the data that you presented on AFM24, maybe a two-part question.

Can you remind us why you think these 3 expand planned expansion cohorts will be most amenable to single agent activity, so that CRC [Indiscernible] The EGFR unit long (ph) and RCC? And then it is, I guess those tumor type where you did see the stable disease or that patient with progressive disease that continues on treatments.

Can you share anything more about those patients that they have high EGFR expression, they were refractory to other easier for targeted therapies. Thank you..

Over to Andreas please?.

Yes. Hi, Dana. Let's start with probably with the second question, second part, first. The patients that we have treated on 480 mg, we have this 2 patients with EGFR mutant non-small cell lung cancer, and a colorectal cancer patients. Important to note, we fixed or we decided which tumor types will go into which off the studies prior to seeing the data.

And as I said, this decision was really driven on this comprehensive analysis that we showed where we looked at the data for more than 10,000 patients. And then really looking at biology cells, innate immune system, activating and inhibiting factors, and case cell biology.

So what we see now here on slide 6 again, very small on at 6, very small patient number. It's a little bit maybe an early confirmation of our selection process.

If you look at the colorectal cancer patients wild-type patient number 1, while this would be a patient who would have qualified for the expansion cohort, patient number 3, EGFR mutant none the more, is another patient that would have qualified, and patient 5. Again, EGFR mutant would be in the patient that would have qualified.

While the other 2 patients, 2 and 4 where we have follow up data, patient 6 is very early in this treatment, and would have not qualified for the expansion cohort as mono therapy. Again, the sequence was different, so we looked at the biology first and then decided which are the most likely cohorts or most likely tumor types that can respond.

Again, with this very small dataset there seems to be a trend that exactly these two most really do quite well on AFM24 mono-therapy. Now, we have measured GFR across all cohorts. Most patients have moderate to high expression.

I don't have individual patient numbers or data, but I would expect us to EGFR mutant non-small-cell lung cancer patients have rose a high expression of EGFR receptor. So required monthly, I needed to exhaust all previous lines of therapy.

All of these patients have been pre -treated and has become resistant to EGFR targeting therapies whether it's TKIs or antibodies..

Very helpful. Thank you..

Thank you. Our next question comes from the line of Maury Raycroft from Jefferies. Your question, please..

Hi. Good morning and good day, everyone. And congrats on the updates and thanks for taking my questions. I had a question on AFM24 2. For that one, you showed a lot of helpful PK and PD data. I'm wondering if you can tie it together with what you're seeing in the 6 patients at 480 mix, particularly in respect to anti-tumor activity.

As you approached steady-state. And if you can talk more about what you're seeing on cytokines and [Indiscernible] [Indiscernible] activation markers as exposure increases..

I can take the first part, let me hand it over to Arndt regarding the cytokines. Sorry, as you see, all these patients are treated at 480 milligrams. So this was the dose level where we achieved a dose proportionality. So we have basically saturated EGFR binding.

As we showed, we also achieved CD16, a receptor occupancy and then correlating figures into tumors that according to our experiments, are sufficient to maximum activation of the tumor residing NK cells. We have not broken downs these data on an individual patient level yet, but this is something that we will have to do in the future..

And maybe.

And Arndt maybe can talk --.

Yes,.

On the NK cell. Yes..

Yeah. Sure. Happy to do so. So you noted Maury, we didn't share that data because we want to disclose that, as discussed at an upcoming conference in '22. What we see, what I can share with you in terms of the cytokines, to give an example, interferon gamma.

If alpha important for NK cell activation at doses is at, or above 160, when we look at the steady-state levels, we see in a steady increase, We didn't see a real difference between 320 and 480, but we see that it clearly was rising above 160, making the point again that this is clearly pharmacologically active in terms of the activation markers.

Similarly, we want to share that data when it's also a little bit more matured, but the same trends that we see at doses above 160, we saw an increase of those activation markers again showing that we have consistent NK cell activation. Hopefully that helps with your question..

That's very helpful. And maybe 1 other question on the AFM13 plus on core blood NK cells combo study. Just wondering if you can talk more about expectations on durability for this upcoming update. And also just checking if you have plans to move this study over to sponsorship at AffiMed at some point..

Andreas, can you take the question please?.

Yes. What you see or what you realize is, when you compare to the status that we have, basically by the middle of the year, June or so, We have added a very significant number of patients over the last couple of months.

I would say that for the highest dose cohort time to progression or duration of response data will be quite immature in December as many of these patients have recently started treatment within the last 3, 4 months.

Of course on the lower doses, we have a longer follow-up but again, this will not be the therapeutic doses set that we will move into our expansion cohort and we'll use subsequently. Now in terms of sponsorship, we have not decided. As we always said we are working on with several CDMOs to transfer the production process.

We are in the process of doing that, and we'll provide updates as we have more concrete dated share..

Got it. Okay, that's helpful. Thanks for taking my questions..

Thank you. Our next question comes from the line of Deborah Canta (ph) from Tourist Securities. Your question, please..

Thank you so much for taking my question and congrats on all the progress. I have a follow-up question on the AFM13, the cord blood NK cell combo.

Can you talk a little bit about the decision to expand into both HL and NHL patients? What should we expect the split to be? Should -- are you looking to enroll more NHL patients? And maybe talk a little bit about how this -- if at all this changes your strategy in what to focus on whether it's HL or NHL. Thank you so much..

Thanks a lot again. Andreas is answering your question. Andreas..

As you know, CD30 is a target that is expressed on Hodgkin's, but also on non-Hodgkin's lymphoma like, like T-cell lymphoma, a subset of CD30 -positive B-cell lymphomas. Currently we are following, if you will, a two-pronged approach.

Clearly, our main indication, or the first indication I would say, will be Hodgkin's lymphoma where we have the wealth of stage and where we have seen this very impressive responses already in the first 4 patients.

The study, is this now designed that it will recruit 30 Hodgkin 's patients at the recommended Phase 2 dose, which we believe gives us a good data set to move on with Hodgkin on the registration path. Now, the second part is a little bit opportunistic.

Again, it has also very significant medical need in peripheral T-cell lymphoma and in diffuse large B-cell lymphoma. So we thought that we at least should explore NK cell based on AFM13 based combinations in these diseases that could potentially result in the second or the second and the third development pathway.

So this is really broadening the indications, but for now, Hodgkin's will be our lead indication, where we will try to move ahead with full steam..

Right. Thank you.

And just a follow-up question on the AFM24, the data that you presented, you've been dose escalating for a while, but have you seen any indication especially with the lower doses or patients have been treated for longer period of time, the deepening of responses?.

We have occasionally seen some disease stabilization a that lower doses. But again, according to our data, the maximum pharmacokinetic pharmacodynamic atttude or activity was set in around 162 sweet 20, was for ADB in our selected dose right now. These are really anecdotal observations.

As we said, out of our 480 milligram cohort, 4 of 6 patients are still on treatment. I think this this will be interesting to cohort to watch, whether we do see a deepening of responses..

Great. Thank you very much..

Thank you. Our next question comes from the line of Nick Abbott from Wells Fargo.

Your question, please?.

Good morning. Thanks for taking my questions and thank you for all the detail on AFM24. First question is on AFM28. Can you speak to why CD133 in the context of the CD-3/CD-33 the case you built for Artiva? We'll compared CD123 to CD-33. And innate-cells to T-cells in this application in AML. Thanks..

You happy to take this question, Arndt?.

Yes. Happy to do that. Nick, yes, we -- I think we already also provided some background information as you [Indiscernible] has this CD33. I think a very valid target, of course, in combination with a CD3 and a T-cell engager. Why are we -- why have we selected, maybe let me speak about a re-trade, CD123.

1 is, it is very broadly expressed on the leukemic blasts. It's also expressed equally Leukemic stem cells and importantly, non-not unhealthy stem cell. So, we have a very high selectivity.

We've also followed our approach in selecting this when we look at, in a way that programs that have been out there like in Fc -enhanced CD123 target antibody that was -- comes from Johnson & Johnson.

A while ago talacotuzumab that was not continued because as an Fc -enhanced antibody, without the additional mechanisms of actions that we believe we add in terms of also the efficacy, in terms of the, let's say, tuning engineering with the molecule we see a great potential to address that medical need.

Indeed, also with those approaches talacotuzumab is the occasional complete responses versus seeing where we are specifically excited is in the prospect of course testing monotherapy of that, but then very quickly combining AFM 28 with Eligen NK cells.

Why? Because we know in AML for a myeloid disease in case of the macrophages will not be at least fully functional or not functional. So adding in a way you could say the payload or mechanism of action with Eligen A NK cell transfer.

We see a very high probability of success to getting to those deeper responses that we're looking at, which is this very high medical needs to really get to also minimal residual disease negative patients, Hopefully that kind of addresses your question, Nick..

Yes. And I think, the point of NK cells, T-cells emphasizes that safety advantage you feel there is where that NK cell, versus a T-cell engage in..

Yes, absolutely. That is an important point. We have now seen consistently across our Innate Cell Engagers. Excellent safety profile, some of the early RAS that we have seen very well manageable schedule, pretreatments. So NK cells are just by the nature of their biology, very effective, but much safer than T-cells again.

I think we know the principle by now. It's not only the cytokine storm, but it's also really the -- in a way alter your immune effects that we see where T-cells once unleashed.

I'm just not selective in kind of targeting for attacking the tumor versus healthy [Indiscernible] NK cells very well distinguish [Indiscernible] thus, very much better safety profile.

And as I laid out, I think when you look at the very elderly patient population that we have rail patients that will not tolerate some of them the high dose chemotherapy. We see this as a very differentiated, good profile with an NK cell engagement..

Okay. And then maybe just last 1 for me. In solid tumors, obviously with [Indiscernible] described very elegantly, a three-pronged strategy. You've already elucidated to an NK cell combos. Press M2016, at least two Pro is there a three-pronged strategy.

Do you think that's applicable for AFM28 Marlow disease?.

That's a really good question. Happy also for Adi or Andreas to jump in. We have currently, also publicly, said we want to make the combination with Eligen NK cell as a priority because of the reasons I have been giving.

There may be cases for also the third pillar that's not something that we have fully thought through and with updates accordingly, as we move on with our plans..

[Indiscernible] Thank you very much..

Thank you. Our next question comes from the line of Brad Kimmino from Stifel. Your question, please..

Thank you. And appreciate the updates today. Just quickly on the protocol amendment for AFM 13 and k, was that driven by MD Anderson or by your team? And if could talk more about the reason behind that. Then I'm also interested in the breakdown of the 6 AFM24 patients you had at the 480 make cohort.

You highlighted how three of these would have been eligible for the monotherapy expansion cohort. But they had 4 to 7 prior lines of therapy. Looks like in the expansion cohort, should we expect this number of prior lines of therapy or will you be looking for patients that are maybe earlier at 1 or 2 prior lines. Thank you..

I guess, Andreas, the first question is for you..

Yeah, so let's start with the amendment of the protocol. I think we're -- importantly, we have a very good, a very close working relationship with MD Anderson, so I would say it was basically a joint effort, joint decision. Initially, the protocol was only designed to evaluate safety.

So it was a pure Phase 1 safety protocol, but then I would say even for us a little bit unexpectedly, we saw this really significant anti-tumor activity already up the lower dose levels and so we immediately developed the desire to gather more efficacy data and to basically put this compound on a development path.

So we use the existing product called to allow for more patients at the recommended phase 2, which will give us sufficient number of patients to really have a good solid estimation of efficacy in Hodgkin's lymphoma.

And as we always said, we'll provide ICE basis to engage with healthcare, with regulators for the most appropriate on success this past towards approval. So this was a joint decision on it was really driven by our enthusiasm, and those MD Anderson, our enthusiasm developed a data that we were seeing.

Now in terms of how the expansion cohorts in study 101, yeah, you're rights as these patients are heavily pretreated. And I think taking this into account of this degree of effectivity in, in late line from at least for us is really very encouraging.

Whether there will be less pretreated patients in the expansion cohort is a little bit hard to site of the expansion. Quartz still requires that patients has exhausted all available treatment options for their respective diseases. So I would say we will see a majority of patients with 3 to 4 lines of previous therapy.

Again, we are [Indiscernible] thing here in an area of very significant unmet medical need, which generates a high bar. And -- but on the other hand, we believe also had fore seen for a potential accelerated approval process if you can show a robust and reproducible activity in patients that have no treatment alternatives left..

Thank you..

Thank you. [Operator Instructions]. And this does conclude the question-and-answer session, as well as today's Affirmed third quarter update call. Thank you, ladies and gentlemen, for your participation. You may now disconnect. Good day..