Good day, and welcome to Affimed's Second Quarter 2021 Financial Results and Corporate Update Conference Call. At this time, all participants are in listen only mode. After the speakers' presentation, there will be a question and answer As a reminder, today's conference call is being recorded. I'd now like to introduce your host for today's conference call, Alex Fudukides, Head of Investor Relations at Affimed. Please go ahead.
Thank you, Liz. I'd like to also welcome you all for joining us today for our Q2 2021 results and operational update call. Before we begin, I'd 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 Hoss, our Chief Executive Officer Andreas Harstrig, our Chief Medical Officer Arndt Utilius, our Chief Scientific Officer Wolfgang Fischer, our Chief Operating Officer And Angus Smith, our Chief Financial Officer. The whole team will be available for the Q and A session.
Before we start, quickly to go through This 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 differ materially from those anticipated in the forward looking statement, even if new information becomes available in the future. These forward looking statements are subject to risks and uncertainties, and actual results may differ materially from those expressed or implied in the statements 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 With that, I'll turn the call over to Adi.
Adi?
Yes. Thank you, Alex, and good morning, everyone. And thanks a lot for joining in for our Q2 update call. Today, we're going to provide an update on our pipeline, Discuss the progress on our ongoing AFM13, AFM24 and AFM28 studies and our plan What promises to be an exciting period over the next few months for our company. Before I do that, a quick summary of what we have accomplished So far, the clinical and preclinical data confirm that our unique And innovative innate cell engagers are safe and have the potential to be effective in treating cancer patients, Both as monotherapies, but also in combination either with natural killer cells or with checkpoint antibodies such as PD-one, maybe PD L1.
As we move the ongoing clinical trials forward, our efforts are now focusing on identifying and targeting indications where we believe our scientific discoveries will benefit patients by applying our 3 pronged approach, Monotherapy therapies in combination with natural killer cells and checkpoint inhibitors. We're very happy to report that our pipeline remains on track for our registration directed study of AFM13 monotherapy in relapsed We are recruiting well and on track to complete enrollment of the study in the first half of twenty twenty two. And we expect to be able to provide further guidance about timing for data as we get closer to the completion of enrollment. In the investigator sponsored clinical trial at MD Anderson Cancer Center, Evaluating cold blood derived natural killer cells pre complexed with AFM13, we have completed the dose escalation part of the study. With increasing doses, indeed there were 3 cohorts where we used either 10 to the 6 cells per kilogram, 3 patients that received 10 to the 7 cells per kilogram and 3 patients that received 10 to the 8 cells per kilogram.
We're currently enrolling additional patients at the highest dose of 10 to the 8 cells per kilogram to gather robust data On safety and efficacy, what would form the basis for discussions with regulators about appropriate approval strategies. No dose limiting toxicities have been observed during the dose escalation in any of the three cohorts, and we remain encouraged The next data update is planned for the Q4 at a major medical conference. Regarding our efforts to take forward the combination of AFM13 with natural killer cells into a registration direct study, we have signed up A CDMO for the manufacturing of the NK cells and have generated additional data on cryopreserved natural killer cells pre complexed with AFM30. As we have shared with you over the past few months, We view this CAR like NK characteristics of our innate cell engagers in combination with natural killer cells as a major advantage over The major difference being that when we look closer at the cell surface retention, Our innate cell engagers won't fall off a combined therapy for a very long time, including days later. Whereas monoclonal antibodies are not retained for very long.
As a result, our research shows That it is not possible to generate a pre complex product with monoclonal antibodies, but with inhaling HS only. Moreover, our research demonstrates that the engagement of our innate cell engager molecules with natural killer cells activates the natural killer cells to kill tumor cells. In our collaboration with the Karolinska Institute, we found that AFM13, When compared to a molecule on the 3,030 antibody mediated a more potent activation of natural killer cells, Leading to a significantly increased number of natural killer cells that exerted engagement with multiple target cells This exciting data has been accepted as opposed to presentation At the SITC Annual Meeting in November. In our ongoing trial with MD Anderson, it is our goal to generate a Strong data package that would support discussions with the FDA and other agencies regarding next steps for the program, including a potential registration directed study. Now let me turn over to AFM24, our EGFR directed innate cell engager.
For AFM24, we continue to execute our 3 pronged strategy of monotherapy, combination with natural killer cells in combination with the checkpoint inhibitor PD L1. Our goal in this program is to evaluate a broad set of solid tumor indications in parallel, supported all by a strong biological rationale. We expect Multiple inflection points this year and plan to have multiple additional data readouts in 2022. Our monotherapy dose escalation study is on track. Based on current data Cohorts 5 and 6 are pharmacologically active doses.
Therefore, we have increased the size of Cohort 5. Patients are dosed at 320 milligram and CORH-six patients are dosed at 480 milligram To generate additional pharmacokinetic and pharmacodynamic data that we expect will aid our selection of the recommended Phase 2 As of today in each of the cohorts, 5 and 6, 5 out of 6 patients are enrolled. It is important to mention that to date in patients that have already completed the DLT period in each cohort, No dose limiting toxicities were observed. So as just mentioned, we continue to see a good safety profile of AFM24. We confirm that we have not seen any of the classical EGFR related side effects like apneaform This is in line with the distinct mechanisms of action of AFM24, which is very different from the mode of action of EGFR pathway targeting antibodies like cetuximab or panitumumab.
These findings also confirm the data from our pivotal toxicology studies in cynomolgos in monkeys that indicated a different side effect profile for AFM24 versus tatuximab. Infusion related reactions remain the main side effect and are well manageable with symptomatic treatment and modifications of infusion rate. The ongoing dose escalation part includes patients with any EGFR expressed in solid tumors. When assessing antitumor activity at those levels in the 320 milligram and 480 milligram cohort, We are encouraged to see that there were several patients on this study that experienced disease stabilization beyond 8 weeks, and you are able to receive additional cycles. Biomarker analysis of the patients Point to the activation of the effector cells shown by increasing expression of activation markers and a continuous secretion of cytokines.
Indeed, supportive of this observation is a continuous occupancy of the CD16A receptor. We are enrolling patients in the monotherapy study and independent of the selection of our recommended Phase 2 dose, We plan to continue to increase the dose in non selected patients to gather further insight into the exposure effect relationship of AFM24 focusing on PD market and to confirm safety of AFM24 at even higher dose levels. Important now to note is in addition, in line with our guidance, we expect now to start enrollment of indication specific patients in the expansion cohorts using single agent AFM24 in the second half of twenty twenty one. These cohorts have been chosen based on a detailed analysis of the tumor biology as we explained in the past and will enrich for patients that we believe have a high likelihood to respond to single agent AFM24. These expansion cohorts include will include renal cell carcinoma that failed standard of care, which includes PKIs and PD-one targeted therapy.
2nd indication is non small cell lung cancer, EGFR mutant failing standard of care, And the 3rd indication is colorectal cancer failing chemotherapy plus EGFR targeted antibody. So we have selected 3 indications for the monotherapy study. In addition, we are now in the final stages Of the setup phase for our combination studies of AFM24 with both atezolizumab, Study is called ASM24102 and the autologous NK cell product SNK01. This study is called ASM24-103. We confirm our guidance that we expect both of these studies to start enrolling patients in 2021.
The tumor types we plan to study with the AFM24, adhesive combination are as follows. Again, non small cell lung cancer, in this case EGFR wild type, failing chemo and PD-one targeted therapy. Gastric and GEG cancer failing standard platinum based chemo And a basket of EGFR expressing tumors comprising pancreatic hepatocellular and biliary tract cancer, Again, failing standard of therapy for the respective species. Now the tumor types we plan to Study in AFM24 SNK01 NK cell combination study are as follows. Again, non small cell lung cancer, EGFR wild type, squamous cell carcinoma of the head and neck, Failing chemo and PD-one and colorectal cancer failing standard of care.
The indications for each of the 3 studies have been selected carefully based on the biology of each tumor type. This approach allows us to investigate a broad set of solid tumors, while also providing multiple shots on goal for the more prevalent tumor types such as non small cell lung cancer and colorectal cancer. In summary, we're very satisfied with the progress of the AFM24 program. The data show that AFM24 Processes a different mode of action compared to conventional EGFR targeting antibody. We see pharmacological activity based on In a receptor binding and NK activation markers.
At these pharmacologically active doses, we see no classical EGFR related to side effects like skinuemercotoxicity. And in addition, we were seeing disease stabilization in these heavily pretreated patients At dose levels 3 20 milligram and 4 80 milligram. We believe in the significant potential of AFM24 and with planned expansion of the program, we're seeking to maximize this opportunity, addressing a broad set of major eGFR expressing tumor indications. And this strategy will allow us to provide a continuous flow of data. Now let me move to the 3rd program, AFM28.
For AFM-twenty eight, we continue to advance the IND enabling studies and have submitted an abstract with initial preclinical data for a major medical conference later this year. We plan to release information about the target and the indication once the abstract becomes available. We remain on track to submit the IND application in the first half of twenty twenty two, Our goal is to begin a clinical study in the second half of twenty twenty two. In addition To moving forward things forward in the clinic, we're continuing to publish data that supports our work. One such example is the recently published preclinical data that supported the IND filing IND application of our innate cell engager ADF M24 In the journal maps.
Arndt, our CSO, will discuss the key takeaways
Thanks, Adi. And also from me, a very warm welcome to everybody The call as introduced by Adi, I would like to summarize the key preclinical data for AFM24 described In the recent publication in the journal MAPS, in this paper we demonstrate the high affinity binding of AFRAME24 to CD16A on natural killer cells and macrophages Its strong binding value is in the low nanomolar range. Importantly, AFM24 binds to CD16A On NK cells, a macrophage with high affinity at a site that is distinct on binding of IgG Such that high concentrations of polyclonal IgG results in a minimal only 2 fold reduction in binding affinity. In contrast, binding of an Fc enhanced high affinity anti EGFR IgG Antibody was significantly inhibited. These data again demonstrate the high surface retention of our ICE molecules 2 NK cells enabling the earlier described pre complexing 2 NK cells with CAR like NK cell properties, which are not possible with normal or Fc enhanced antibodies.
We also show high affinity binding of 1824 or in the nanomolar range to various EGFR expressing tumor cells AFM24 demonstrated to be highly Differentiated from marketed anti EGFR antibodies with its ability to potently and effectively kill tumor cells Through antibody dependent cell mediated cytotoxicity or ADCC are NK cells. Moreover, this ICE mediated potent antibody dependent cellular fibrocytosis or ADCP by macrophages in vitro. AFM24 was also shown to be effective towards a variety of EGFR expressing tumor cells, killing these regardless of their eGFR expression level and irrespective of their KRAS BRAF, BRAF, mutational status. In addition, SA-one hundred and twenty four has a lower Affinity for EGFR and binds to a different epitope than cetuximab. It exerts an over 1,000 fold Lower inhibitory activity on EGFR signaling further underscoring its highly differentiated mechanism of action.
Now in terms of envivosator in tumor mouse models, we have published at AACR, this year's AACR showing dose dependent anti tumor This anti tumor activity for AFM24 or in combination with NK Cells has now also been demonstrated with pre complex and cryopreserved NK cells in vitro and in vivo within one of our preclinical collaborations. This exciting data gives us confidence That the NK cell product we used in combination with AFM24 retains its potent antitumor activity after Try preservation in vitro and in vivo. Now coming to the toxicology studies, Incinomonkey is also described in the paper, AFM24 was well tolerated up to the highest dose of 75 mgs per kg When administered once weekly for 28 days. Remarkably, skin and other cytotoxicities, Which had been observed in these dose levels with cetuximab and comparable Sino monkey studies were not observed here. Only transient elevation of interleukin-six levels was detected at all dose levels, which returned to baseline after 24 hours.
Moreover, an increase in circulating CD40 monocytes was observed after the first dose of AFM24 concurrent with a decrease of circulating NK cells at doses of greater or equal 8 milligrams per kilogram, now view showing the expected pharmacodynamic effect of this drug candidate. Taken together, these results emphasize the promise of our bispecific innate cell engagers as an alternative cancer therapy And demonstrate the potential for AFM24 to effectively target tumors expressing various Varying levels of EGFR regardless of their mutational status. Happy to answer any questions you may have about this in our Q and A. And for now, I'll hand The call over to Angus to review the financials. Angus?
Thank you, Arndt. Appiumed's consolidated financial statements have been prepared in accordance with IFRS as issued by the International Accounting Standard Board or IASB. The consolidated financial statements are presented in euros, which is the company's functional and presentation currency. Therefore, All financial numbers that I will present in this call, unless otherwise noted, will be in euros. We ended the Q2 of 2021 with cash and cash Equivalent of €222,700,000 compared to €146,900,000 on December 31, 2020.
Based on our current operating plan and assumptions, we anticipate that our cash and cash equivalents will support operations into the second half of twenty twenty three. Net cash used in operating activities for the quarter ended June 30, 2021 was €17,300,000 compared to €15,000,000 in the Q2 of 2020. Total revenue for the Q2 ended June 30, 2021 was €9,700,000 compared with €2,900,000 for the quarter ended €7,000,000 compared with €2,900,000 for the quarter ended June 30, 2020. Revenue for the Q2 of 21 mainly comprised of collaboration revenue from Genentech and Royvant. Research and development expense for the Q2 of 2021 €21,800,000 compared to €11,700,000 for the Q2 of 2020.
The increase in R and D expenses compared to the same period last year or driven primarily by increased expenses for AFM24, including costs for the production of clinical trial material as well as an increase in costs associated with our other early stage programs and infrastructure and an increase in share based payment expense. General and administrative expenses for the Q2 of 2021 increased by 109% to $5,400,000 from 2 point 1,000,000 in the Q2 ended June 30, 2020. The increase relates largely to higher personnel expenses, higher premiums for our directors and officers liability insurance, Higher consulting expenses and increased share based payment expenses. Net finance costs for the quarter ended June 30, 2021 increased by 63 From $1,000,000 in the quarter ended June 30, 2020 to $1,600,000 during the Q2 of 2021. The increase is largely due to foreign exchange losses related to assets denominated in U.
S. Dollars as a result of the weakening of the U. S. Dollar against the euro during the quarter. Net loss for the quarter ended June 30, 2021 was €18,800,000 or 0 point 1 $6 per common share compared with a net loss of €12,200,000 or 0 point one six dollars per common share for the quarter ended June 30, 2020.
The weighted number of common shares outstanding for the quarter ended June 30, 2021 was 119,600,000. I will now turn the call back to Adi for closing remarks. Adi?
Thanks a lot, Angus. As just explained, our company is making significant strides forward by advancing science and demonstrating that our innate cell engagers can play a leading role in enabling innate immune cells to identify and eliminate cancer cells. Now for AFM13, our strategy development strategy allows us to target a broad set of CD30 positive Lymphoma, indeed including various types of non Hodgkin and Hodgkin lymphoma. We're very excited about the potential And market opportunity for AFM13 in these indications and we will have additional data for the NK cell combination study by the For AFM24, we're now executing a strategy that We believe it gives us the highest probability of success. We have reached active dose levels in our dose escalation study And we'll now use this to initiate this 3 pronged development approach in parallel, indeed Across a broad set of solid tumor indications.
We expect that these three studies will generate a continuous flow Finally, we are executing on our preclinical pipeline to bring additional product candidates into the clinic. Our development progress for AFM 28 is indicative of our ability to further expand our pipeline By leveraging the unique ROCK platform and we're working on additional early candidates from the platform. Many, many people have contributed to bring our innovative therapies to patients who need additional options in their fight These include patients and their families who entrust us with the lives Of the loved ones, our employees and the investors who over the years have supported our efforts. As always, I'm very thankful for the trust you put into our efforts. Thank you.
We're now ready to take any questions that you may have. Operator?
Our first question comes from Dana Graybosch with SVB Leerink.
Hi, all. Thanks for the question and for the pretty Nicely comprehensive call. 2 for me on AFM24. The first is, I believe you mentioned, and I just want to confirm that you saw Stable disease in several patients beyond 8 weeks. And in that same sentence you mentioned that you're recruiting any EGFR expressing solid tumors.
I'm wondering if you could clarify whether you saw the stable disease in patients that had more EGFR expression. Was there any correlation with that? Or even if you could tell us of these patients recruited at Cohort 56, what proportion of them did have high eGFR Which ended up with low eGFR? That's the first question. And the second question is, can you confirm how you ultimately will select a dose Given you haven't hit any dose limiting toxicity, can you will you be going off pharmacodynamic activation In the periphery, what gives you confidence that, that will track with your activity in the tumor?
Will you be going off of Occupancy of CD16 or eGFR or will you continue to try to dose as high as possible until you do understand your highest tolerable Thank you very much.
Thank you, Dana. I have to check if Andreas is still on the phone. Andreas, Could you follow the questions? And okay, very good, Andreas.
Yes. I'm on the phone. I I apologize. I'm in rural Italy. So if I break up at some point, it's due to technology reasons.
But I try to Stay as long as I can. So let's start with the second part of the question first and Arnd also chiming. So as we always said, the selection of our recommended Phase 2 dose will be based on pharmacodynamic markers. As Arnd mentioned, our mechanism of action is completely different from EGFR pathway targeting agents Like cetuximab or the TKI. So we were not expecting to see any dose limiting toxicity like skin or mucosa.
And what we're seeing clinically is really reconfirming this assumption. So IARs remain the side effect, which are well manageable, We are not seeing any skin toxicity, any mucosal toxicity. As we said in terms of pharmacodynamic markers, we have A whole array of parameters that we look at, the most leading parameters are Marcus of the activation of circulating NK cells as well as the occupancy of the CD16A receptor, Where we see values that are well above those values needed for Experiment activity are in vitro and in vivo. So we feel very confident that we are currently working at And this is our doses that we will take forward into Phase 2 testing both as a single agent as well as recombinations. Irrespective of this, we may Delay 1 or 2 additional dose steps just to confirm that we have a very good safety profile, a very good But not necessarily to use this higher doses for further evaluation of clinical activity.
In terms of eGFR expression, we are collecting the data Again, for the highest dose levels, we have not all data in house. For the lower dose levels, we could not see any correlation between the
Got it. Thank you very much.
Our next question comes from Maury Raycroft with Jefferies.
Hi, good morning, everyone. Good afternoon and congrats on the progress. Also one question on AFM24, you mentioned additional inflection points for the Just wondering if you can recap what those inflection points are?
Yes. So as we've mentioned, we are now planning to Start the dose expansion cohort. So that's an important milestone. And we've also mentioned There are 2 additional studies that are being initiated. The one is the combination So these are 3 Very important inflection point in our mind.
And in addition, we can provide updates As we proceed with the dose escalation study, you have heard from Andreas that we have Expanded the Cohorts 56 to include more patients, those data will be collected and analyzed. And once available, We plan to share this data with you.
Got it. That's helpful.
Maurice?
Yes. Yes, I'm still here. And just wondering if you're saying anything additional about any more specifics on the Activation markers and cytokine secretion that you're seeing, if you're providing any more specifics.
Arnd? Yes.
Thanks, Maury. Good question. At this point, not specifically we would like to share that. I mean, we have said, just Repeat maybe what Andreas already said. We look at activation and exhaustion markers on circulating NK cells.
We look at infiltration of the cells in some of the biopsies we have. We look at the cytokine levels. And of course, as we have reported, in addition to exposure, so PK parameters also at receptor Occupancy and we will share that in more detail once all the data is, as Adi also mentioned, will be We've collected together and then we'll also share the specific markers used.
Got it. Okay. And then also wanted to ask about the AFM13 plus NK cell combo. Can you say if you have responses at the highest dose At this point and how many patients total at the highest dose are planned for the study?
So we haven't disclosed any such details for the time being as we are preparing for a Presentation later in the year as outlined so that we can see the composite. But in short, what the plan has We have in each cohort initially 3 patients and a cohort is always A certain number of NK Cells, which is increased by a factor of 10 when the safety is warranted. And As I said, it's 10 to the 6 cells per kilogram. We moved to 10 to the 7 and 10 to the 8. In these patients, we haven't seen any Those limiting toxicities or any other side effects appears quite safe.
And overall, What I can see here is that we're also very encouraged by the responses that we're seeing after the first assessment. Currently, additional patients are treated. So we have continued to enroll patients. Our MD Anderson has continued To enroll patients at the highest dose cohort and that's currently ongoing.
Got it. Okay. That's helpful. And then my last question and then I'll hop in the queue. In the prepared remarks, you said the program, the AFM13 plus NK cell combo program Would be robust and could enable discussions with regulators for approval strategies.
I'm just wondering if you think you'll have enough data by year end 2021 to
In terms of timing, we've been we will let you know as soon as We have such data. It's an IST, so we're dependent on MD Anderson to enroll these patients. And so I would say that we have to wait for a little while before we can confirm any of these next activities. This is an important activity, but as we feel it's not the only very important activity. The other one is that We can proceed with the NK Cells and its manufacturing.
And I was sharing 2 news today that we have made good progress On this front as well, first, we're now working with the CDMO for the manufacturing of the co blood derived NK Cells, and we have generated first data of a cryopreserved AFM13 pre complexed NK cells and determined its activity In preclinical experiment.
Got it. Okay. Congrats again and thanks for taking my question.
Thank you.
Our next question comes from Nick Abbott with Wells Fargo.
Good morning. Thanks for taking our questions. And rural Italy sounds delightful, I have to say. Just Starting off maybe on AFM13. You mentioned the CDMO, Adi.
Is this using cord blood from MD Anderson? Obviously, I know that you've licensed the technology from them, but Are you restricted to where the cord blood cells come from, which bank they come from?
So yes, we have a license to the entire technology and this would also include indeed any work On the cryopreservation that's being conducted by MD Anderson. In terms of core blood cells, we're not restricted To any specific source, so we can source this from MD Anderson, but also independent places. And so in essence, that's how we are set up. Is there a specific reason why you're asking?
No, not at all. No, at all. I was just thinking if you were going to be we don't know where the CDMO is, but if you were going to have a CDMO in Germany, for example, and Shipping cord blood from MD Anderson when it is convenient and sourcing it from somewhere in Germany.
Yes. No, it's an international CDMO, so that has footprint All over the world, it's obviously one of the very experienced ones that was important to us. Again, on the CDMO that has already Worked and Developed NK Cell Products. So we're tapping into specific know how already With this choice and at the moment, our focus is to work with the science in the U. S.
Okay, great. Thank you. And then just on AFM24 and terrific now to finally give you details of those expansion cohorts. One thing that struck me in monotherapy, there's not a KRAS mutated colorectal cohort. The AK combo would appear to allow for KRAS mutated colorectal, but did you consider is there a reason why there isn't a KRAS mutated cohort, obviously, couldn't be EGFR pretreated and that's probably the reason, but I thought I'd ask.
Andreas, can you help out here?
Yes. This is a good pick. As we said, Our selection on the expansion cohorts are based on a pretty thorough analysis of The underlying tumor biology and the makeup of the different players of the innate immune system. When we look specifically at KRAS mutated colorectal cancer, it's not due to the KRAS mutation, but there appears to be a coincidence that Many KRAS mutated colorectal cancers have very limited To us, KRAS mutated colorectal cancer would be one of these indications, where the patient would need support of an And that's the reason why they ended up basically in Study 103. We believe that once you are able to Supply these KRAS mutant colorectal cancers with NK cells and with an appropriate engager All that supports the innate immune system in the best position to work against is very difficult to treat tumors.
Sorry. Thank you very much. I'll hop back in the queue.
Our next question comes from Dale Chen with Laidlaw.
Good morning and afternoon and thanks for taking the question. The first question is for the FM13 plus the Core blood NK cell, which that according to clinicaltrial dot gov that you have They expect to include about 30 patients. Is this target still What do you anticipate or how has any modification on that? And whether that potentially Could be a critical mass for potential sort of registration discussion with FDA.
Andrea, you may want to take that?
Yes. So the first thing that I can confirm is That the protocol is written in a way that we, in fact, can recruit somewhere between 30 and 40 patients At the recommended dose level, this could be a mixture of Hodgkin's and non Hodgkin CD30 expressing lymphomas. Again, whether this mass or with this number will be sufficient for any Registration package, of course, will depend on the effect level. And Definitely, this study will allow us probably even earlier than Going up to the full recruitment to engage in discussions with FDA. And I think during these discussions, we will learn What kind of patient numbers are you expecting?
So I think it's a robust study. It will give you a pretty good data set. We will enable us also to look at different biologies within the CD30 expressing lymphoma space. Everything else will really depend on our initial discussions with FDA.
Great. That's very helpful. And maybe just a quick follow-up on this, Which is that, is the data anticipated reporting at ASH or other venues?
Again, the disclosure policy is mainly driven by MD Anderson. Our expectation is that I We'll submit some of the data for ASH.
Okay, great. And maybe one general question for the AFM24. You have the monotherapy as well as The combo specifically with NK cell combo, I noticed that the renal cell carcinoma was only Monotherapy, but not on the combo. Is there any reason behind that or maybe more specific reason behind that?
Yes. The answer is, again, it's based on the analysis of biology And the setup of the different players of the innate immune system, clear cell carcinoma, renal cell carcinoma, we know already Since we took your own time, that this is a tumor there where the immune system can exert some tumor control. When we specifically looked at the players in the innate immune system, we found that RCC is a good candidate that could benefit From monotherapy, so our first step here is to test monotherapy AFM24. We believe that several important pieces are in place in RCC that an innate cell engager could work as a monotherapy. Of course, if we should see good data that would not preclude it at some point, we may add combination with an NK cell or PD-one.
But again, for the first evaluation, our system looks as well as just tumors where monotherapy could be quite beneficial for these patients.
Okay, great. And then maybe the last question, which is a housekeeping one. In the Q2 of this year, the R and D expenditure as well as Revenue has increased, particularly R and D expenditure increased quite significantly compared to the prior quarter. So should we for modeling purposes, should we anticipate the 2nd quarter R and D expenditure will be something more As a base moving going forward for at least for the remaining of the year. And thanks for the Yes.
Thanks, Yale. So I mean, I've got a couple of comments there. I mean, one, we haven't provided specific guidance on our expenses, but we have provided guidance on Our cash runway and what we've said is that we expect our existing cash, which is about a little over €220,000,000 will last That's into the second half of twenty twenty three. So if you do the math on that, again, that's kind of 8 to 10 quarters out. That implies a cash burn in the low to mid-20s excluding any impact of additional proceeds Loans or milestones, etcetera.
So just doing based on that math, you can assume that the Expenditure levels that you're seeing in Q2 of this year is probably more relevant as we go forward than the expenses We've seen in previous quarters, in particular, the Q2 of last year. But having said that, we do expect that R and D expense We'll be lumpy, right? This quarter, we've had, as I said on the call, we had an increase in AFM24. A lot of that's associated with Production of clinical trial material for our ongoing study and upcoming studies. We've also had ramp up In our earlier stage programs like AFM 28 and AFM 32.
And when it comes to CMC investments, So those can be a little bit lumpy, but long story short, fair to assume that the R and D expenditure This quarter is probably more in line with where we'll be in the future than where we've been in the past.
Okay, great. Thanks a lot. And again, congrats for a lot of progress here.
Thank you.
We have a follow-up question from the line of Nick Abbott with Wells Fargo.
Great. Thanks for taking the follow-up. And Just going back to the AFM24 trial, I believe that currently the trial is being conducted at 4 sites in the U. S, U. K.
And Spain. And Adi, you mentioned a U. S. CDMO. So can you talk maybe a little bit about The for the 3 expansion cohorts, how many sites that you Expect to be running those trials at and whether they're going to be international or all in the U.
S. And Will this be Simon's sort of 2 stage design for each of the cohorts? Thanks. Okay. Yes.
Thanks for this question. Nick, I'll have either Wolfgang or Andreas jumping in here if they can.
Yes, I can. So for the expansion cohorts of the monotherapy trial, We are looking to increase the number of sites from 4 that we are currently having probably to Somewhere between 1015, 2016 sites will continue to be a mix Sure. Of our U. S. Site, international sites, you mentioned currently we have Europe.
We will add A couple of sites in Southeast Asia, mainly Korea, especially to recruit EGFR mutant patients. Now the same is true for the PD-one, PD L1 study, where we will have also a mixture of U. S. And ex U. S.
Sites, our Study 103, the SNK-one study We'll initially be a U. S. Only study with up to 4 sites for the initial part and then expanding To cover off more sites, but currently the plans for this specific study are to be a U. S. Only study.
Now in terms of the study design, all studies are designed according to SIMON 2 stage principles. We will have an initial phase with a defined number of patients. Of course, As we are growing different disease types, the go no go criteria will vary by Disease type and then also the definition of final response rate of interest will be a little bit different. But in general, We'll be signing 2 stage designs with an initial cohort of probably around 12 to 15 patients Looking at the predefined success criteria and then having the ability to enroll up to 30 35 patients per cohort to verify the initial assumption of the alcyne and 3 stage design.
Great. Terrific. Thank you very much.
And that concludes today's question and answer session. Ladies and gentlemen, thank you for participating in Affimed's 2nd quarter 2021 financial results and corporate update conference call. This concludes the program and you may now disconnect.