Hi, and very welcome, everybody who joined our webinar today. My name is Andreas Schmidt. I'm the Chief Medical Officer of Heidelberg Pharma. Today, we want to share with you some exciting new news about our clinical development. As you might know, we are developing a clinical asset, which has recently achieved a point. I think you will learn today about this new data in our clinical program. First things first, on top of that, again, I'm thanking all of you who have joined this session. What is Heidelberg Pharma and what is our technology? Those who might not know that, we are developing a new mode of action, a novel ADCs. These ADCs have shown already really positive signs in the clinical, which means that it led to definitive responses in a couple of myeloma, in a few myeloma patients. What is new about this ADC is that this ADC has a new payload. As of today, we are the single developer of this new type of ADCs, which is well protected with our patent families. We know that the payload makes a difference in ADCs. If you change the ADC payload, if you optimize the ADC payload, you can achieve wonderful results as we did in our clinical studies. On top of the new mode of action, which I will tell you a little bit more today, this ADC has a premise that it's specifically active on 70 patient populations. As you know, this is a general issue in oncology, not just in multiple myeloma, but also in other solid tumors and hematological malignancies. Today, we will talk specifically about our lead compound, our flagship compound, which is the HDP-101. What is HDP-101? It is an ADC, which is designed by us. The backbone antibody is targeted to BCMA, the B-cell maturation antigen, which is a well-known target in myeloma, which has superb results in other treatment modalities, including ADCs, CAR T cells, and bispecific molecules. What we did, we attached a new molecule, a molecule which was never before used in the clinic, which is α-amanitin. α-Amanitin is coming from nature. It comes from the desiccated mushroom, and it is a well-known toxin in nature, but so far, nobody was able to exploit this drug as a drug in clinic. What is completely new, that the target of this payload, the target is the inhibition on RNA polymerase II. And RNA polymerase II is an essential cell cycle-independent element, which is, which is a eukaryotic function. It produces mRNA. If we shut down RNA polymerase II, the cells cannot produce, synthetize new proteins and, and goes to apoptosis. Why I'm saying this is cell cycle-independent, it has nothing to do with cell division. Therefore, this type of ADCs can kill dormant tumor cells, which is not true for other currently on the market or in development ADCs, which are using more like chemotherapy, classical chemotherapy origin payloads. Because if it's a new mode of action, it circumstance, and we currently known resistance mechanism, and we can produce this payload synthetically, and we attach it to the ADC. Because it's so powerful, we keep the drug antibody ratio exactly by two, because we know that the rate limiting is really for each and every cycling, the rate limiting is the amount of RNA polymerase II in the cells. So much about the introduction. Now I hand over this presentation to Professor Marc-Steffen Raab, who is one of our principal investigators and who was contributing a lot to this development and still contributing a lot to this development. I think he's more capable to explain to you and put into perspective our clinical results. After his talk, I will also give a short summary on our current achievement and development. I think we should hear first Professor Raab's interpretation of our clinical data. Good morning or good afternoon. I'm Mark Raab from the Heidelberg Myeloma Center, and I'm happy to share the most updated data on the development of HDP-101 in multiple myeloma. Multiple myeloma is a bone marrow microenvironment disease originating from plasma cells that has around 180,000 patients currently worldwide, and most of them still actually succumb to the disease at the end. The current tremendous progress in therapy and therapeutic options, namely with the T-cell redirecting therapies like bispecifics and CAR-T cells, are still considered not curative for almost all patients. Even the most advanced standard of care options largely lack curative potential. Furthermore, those just mentioned treatment options, the most advanced ones like T-cell redirecting therapies, are largely bound to large experienced centers like academic hospitals or huge specialized centers. For example, however, in the U.S., almost 85% of all patients are treated in a community setting like office-based physicians or small community centers. In this regard, HDP-101 and ADCs in general address a high unmet need for this patient population. Briefly, what is HDP-101? It's an anti-BCMA antibody directed, as I said, against BCMA, a surface antigen on myeloma cells. It has a payload with α-amanitin, which constitutes a toxin that is single, that is first in class and has no known other resistance mechanisms so far. The mechanism of action is unique. ADCs in general are very suitable for administration in community hospitals, in outpatient settings, and, for example, as well, in patients who relapse after T-cell redirecting therapies. Other myeloma patient populations that are difficult to treat in general, even with T-cell redirecting therapies, are high-risk cytogenetic, high-risk myeloma in general, older age with comorbidities and frailty indexes, rapid progression requiring off-the-shelf options, so not feasible for CAR-T cell therapy, for example. As I mentioned, the broad availability and simple logistics in many parts of the world, even in advanced countries like the US or Europe. ADCs in general and very specifically HDP-101 offer very convenient dosing regimens and safety aspects compared to the bispecifics and CAR-T cells. As I said, outpatient administration is very feasible for this class of agents. The off-the-shelf availability is much better than especially for CAR-T cell therapy. Non-T-cell approaches are now also again needed after the vast, exploration of the T-cell redirecting therapeutic approaches. Of course, the great opportunity to combine the standard of care drugs and combination regimens is absolutely paramount in multiple myeloma, as has been shown for many decades now with several combination regimens very successfully advancing therapies. Very specifically for HDP-101, there seems to be no ocular toxicity, which is very different from other ADCs, especially one ADC that is already approved, but with limited use because of the side effects. As we have published previously, HDP-101 is able to overcome quite some resistance mechanisms in multiple myeloma. You can see on the left graph here, it is well able to address and to kill efficiently resting non-dividing myeloma cells, which is actually especially in the remission setting and after induction therapy, for example, probably the most important population of myeloma cells in the patient, finally leading later to relapse. As well, it is very efficiently able to kill myeloma patient cells that are derived from myeloma patients who were resistant refractory to existing standard of care combinations. It was also able to kill patient cells with a very low expression of the target antigen on the surface, which is also important because some T-cell redirecting therapies might lead to some downregulation on the surface of the antigen. This is important to know. The HDP-101 phase I-II trial that is currently ongoing has, of course, the objective to explore safety, tolerability, and to find the MTD and the RP2D doses. Up to now, we have solid data, up to cohort seven, as you can see. In cohort six, we introduced a dosing regimen optimization strategy, which I will allude to a little bit later. The key eligibility criteria, as you can see here, were that those patients had to have exposure to standard of care drugs that are available for multiple myeloma and largely did not have any other promising and efficacious alternative available. So far in the dose cohorts five to seven with the relevant doses between 90 and 112 mg per kg, you see with the green and red bars here in the swimmer's plot, you see that we see already quite some remission, quite some durable remissions also in patients, again, in this very heavily pretreated patient population, with the patient here, for example, in the 100 mg dose, reaching a complete remission lasting more than two years, and other patients in this advanced patient population achieving a partial response that is also durable for more than a year in some patients. Let me quickly introduce you to this patient at cohort five, as I alluded already in the previous slide to. This was a 70-year-old lady that already had the diagnosis of multiple myeloma in 2002. Up to enrollment, she had nine prior lines of therapy. Basically everything that was available, including BCMA, CAR-T cell therapy, and the GPRC5D bispecific antibody and iberdomide, a new CELMoD class, in combination with DEX, which she had immediately prior to enrollment. Almost all available therapies and all promising and efficacious therapies have been applied in this patient. In 2023, she was enrolled in HDP-101, in the HDP-101 trial, achieved a PR or partial remission already after two cycles. By the end of the first year, a stringent complete remission could be confirmed. Overall, the treatment was very well tolerated, mild, adverse events, no keratopathy, so no eye tox, no liver damage or lung toxicities were found, and no renal toxicities were reported. There was only one transient thrombocytopenia in the first cycle, which recovered quickly. Actually in the same cohort, cohort five, we found a general phenomenon, obviously, that most patients had a very transient but quickly onsetting dip, so to say, in the platelets, so thrombocytopenia around day five. This is days, not weeks, which recovered quickly a few days later. However, that reached grade three or four toxicity level. We had one patient with some short-term, transaminase elevation in the first week, after exposure. That led to a strategy in cohort six with adjusting the dosing regimen in three different ways. One with a pre-medication, another, so in RMC, so to say, with a weekly dosing instead of the Q3 weekly dosing, and an RMC, a third regimen, for dose optimization, where we split the first dose only, to once weekly, so day one and two, and eight. After that, we resumed three weekly dosing thereafter. That was set up to explore whether the thrombocytopenia, the early dip in platelets, and maybe the liver enzyme elevation, which we saw in one patient only, could be mitigated using those regimens. As you can see here, on the right side, cohort seven, cohort five, you have seen this graph as a comparison before. Cohort seven, as you can see here, we did not see any of the platelet dips in the early days after first administration anymore, both in the weekly dosing as well as in the split dose for the first dose only, and then the Q3 weekly, Q3 dosing, Q3 weekly dosing after that. This adjustment in dosing regimen, which is actually a minor adjustment, if you have split only the first dose and give some pre-medication, successfully mitigated this thrombocytopenia phenomenon we saw in cohort five, even at a higher dose. Very importantly, of course, it did not affect efficacy. Yeah, you see that, the cohort six with the split dosing and the dose adjusted and regimens, with 90 mg per kg, but also in the higher cohort, the cohort seven that I just showed you, we continue to see responses, despite having now split doses or Q weekly dosing in place. That led us to focus in the cohort eight now in only two different scheduling regimens or dosing regimens. One with a Q1 dosing and one with a split dose in the first dose only and pre-medication to be taken further in exploration. The cycle or cohort eight with 140, so still in dose escalation, 140 mg per kg now, and this is very up-to-date data as of two weeks ago. Basically, we saw that we see in four out of those seven patients early responses, as you can see here in green, the partial responses, and even early on in the first three cycles, two patients already achieved a stringent complete remission. Very rapid responses in the majority of patients, again, in a very heavily pretreated patient population that was basically devoid of other options, therapeutic options available. I would say equally important to the great response rates that we seem to see in this cohort, there does not seem to be the platelet drop, the thrombocytopenia in the first few days to occur, as you can see here on the early graphs here now on the platelets. Some minor dips, but that recovered quickly and does not reach, really like high-grade thrombocytopenia. Similar to the liver enzyme elevations, we see in one patient a very minor slight elevation for a few days, but that is then mitigated later on, and no higher-grade liver enzyme elevations, in terms of liver toxicity or something like this, can be detected even at the 140 mg per kg dosing schedule. Overall, in terms of side effects, you see that if you consider grade three, four side effects across all cohorts so far, you see overall very relatively few high-grade grade three, four toxicities, and those were mainly hematological in nature, mainly, of course, with thrombocytopenia as expected as well. I have shown you just in the previous slides, and some anemia, which are of course very common as well in heavily pretreated patients like myeloma, fourth, fifth, sixth line. More importantly, although longer follow-up is certainly needed in cohort eight with 140 mixed per kick dosings, the highest dosing so far, we did not have any grade three, four side effects so far. No early high-grade toxicity at all is being found in this highest dose cohort with the, as I showed you, dosing regimen adjusted to split dosing. Importantly, again, no ocular or renal toxicity has been found so far, and the dip in platelets has been mitigated by the adjusted dosing regimen. Also, interestingly, importantly, for those patients who have exceeded 12 months of therapy, we do not see any cumulative or delayed toxicity. It is not going to have a long-term cumulative effect in terms of thrombocytopenia or any other damage we can see. No lung toxicity seems to occur so far. Again, summarizing across all cohorts the response rates. All cohorts taken together so far, we have a 38% overall response rate with a few patients reaching even complete remissions. Very promising, the highest cohort now, cohort eight with 140 mg per kg, we see four out of seven patients, so 57% of the patients responding, and almost 30%, so two out of seven, reaching a CR within the first three cycles. Clearly exceeding what we have ever seen with any ADC in myeloma in the single-agent advanced patient population setting. Let me summarize the unique features of HDP-101 and what those features might have in terms of potential benefits for patients. As I have shown you, HDP-101 is highly effective against non-proliferating dormant myeloma cells. It is highly effective against myeloma cells that have very low BCMA expression on the surface. It carries a novel mechanism of action with the α-amanitin, to which all patients will be naive, treatment naive. It has so far a very favorable safety profile, especially now after split dosing in the first cycle. Therefore, it is very prone to be very active and easy to combine with other standard of care therapies, which, as I said, has been very important in myeloma in the history so far of drug development. All that might lead to really strong, deep, and long-lasting tumor responses, overcoming resistance acquired by previous lines of therapy, and therefore, especially in combination, leading to a best-in-class efficacy and tolerability profile in multiple myeloma, not only in the relapse refractory setting, but also in early relapses or potentially, of course, even in front line later on in combination therapy. This is all especially true if you compare it to already available ADCs in multiple myeloma that are now on the market and their specific features. With this, I thank you for your attention, and I'm happy to take questions. Ladies and gentlemen, at this time, we will begin the Q&A session. You can ask questions in writing via the Q&A button below the presentation window. I will then read the questions aloud. We've also received a number of questions ahead of the webinar, and I will start with one of them. The first question is, the presentation on the eighth cohort shows that the responding patients are not from the post-BCMA population. Current plans target approval for use specifically in the post-BCMA patient population. However, the current data, while admittedly very preliminary, do not appear particularly promising on this. Could you comment on that, please? Yeah, thank you so much. First of all, I thank Professor Raab for this really excellent summary. Before I answer this specific question, I will also ask you to, there is still time to ask your questions. Please do not hesitate to post your question into the webinar. We will try to address most of them. Regarding these specific questions, yes, our study currently is not limited to post-BCMA or BCMA naive patients. We accept for the dose escalation, we accept both patient population. It is true that for the monotherapy development, we will pursue most likely the post-BCMA field, but we're still considering and actually planning to develop this drug in BCMA naive patient population in earlier lines of treatment, either combination treatment. Generating data in both population is important for us. Because we do not control, we cannot control how many patients we will have who are BCMA naive or post-BCMA in a particular cohort. It is just really as the patients are getting into the study. Still, in the BCMA naive patient population in the last cohort, I think four responders in such a small cohort is quite substantial, especially if you compare it to the early results from other ADCs. This is really something that is outstanding and gives us confidence to further develop this drug as a monotherapeutic agent, particularly in both BCMA naive and post-BCMA settings. Next question, please. Is it correct that fast track status is generally applicable and does not refer specifically to a post-BCMA patient population? Yes, this is correct. We got the fast track designation just recently. This does not specify the BCMA status. It is written as the first line plus patients who received the majority of the currently available myeloma treatment, not including BCMA-directed drugs. Okay. Next question is, to what extent should or could the positioning of HDP-101 and study planning be reconsidered? Is it an option to aim directly for the third line of treatment and position HDP-101 as the first choice BCMA therapy? Would this significantly change the scope or schedule of the study? This does not have a change or any impact on the current scope of this ongoing phase I dose escalation first in human study. However, we already have, and I will demonstrate to you after our Q&A session, I will have some slides on our current development plan. This development plan includes development in the post-BCMA field and also development in BCMA naive earlier lines, which is particularly second line of treatment. Those who have not received any prior BCMA drug. We also, because of the 17p deletions I briefly mentioned in the beginning of our presentation, also plan to develop this drug in the high-risk patient population where we know that the number of 17p deleted patients is higher. Thank you. Next question is, currently, as far as I can see, the 17p deletion population is no longer being mentioned to any great extent. Do you have any 17p deletion patients in the ongoing phase I? Are you planning to integrate this patient cohort into clinical trial planning? Yes. Currently, we do have 17p patients with 17p deletions. As you know, the definition of who is 17p deleted has recently been updated. As our original plan, we still would like to enroll and further test all of our patients for 17p deletion with a fresh tumor biopsy. To report anything meaningful for that, we need a larger cohort of patients. That is why we plan only to report this data after the phase IIa part of the study is completed. We want to do a subgroup analysis on, if possible, a subgroup analysis on this particular patient population in the phase IIa setup. As I said, we also plan to have studies, specifically studies, maybe already pivotal studies in the high-risk myeloma population, which we all know is quite, there we all, that we see quite often 17p deleted patients. Do we have any further questions? Yes. So how many of the patients that were not reaching the stringent complete response status in the former cohorts have died shortly after stopping treatment? As of today, we have not released this data, but as of today, it is a definition of what is short. As of today, we have no knowledge on any patients who passed away quickly after stopping the studies. Obviously, we are following up each and every patient for survival data. Again, this data will be reported at the end of the study when we have a more robust and larger set of patients. As a reminder, if you would like to ask a question, there is a Q&A button below the presentation window, and you can submit your questions there. Next question is, α-amanitin payload on HDP-101 eventually will be released into the system after the affected cells go into apoptosis. As such, it is expected that it will be cleared in the liver and cause some hepatotoxicity. Is there a hypothesis why there are no liver-associated side effects? Yes, excellent question. Yes, the assumption is right that α-amanitin, after it does its job and kills the myeloma cell, is released into the circulation. As of today, if you saw our previous reports and posters and presentations, we continuously reported that we have not measured three, we were not able to measure three payloads. We measure actually three different kinds of payload variants, but we were not able to measure any of them, or when we were able to measure, the amount of these payloads was really minimal. Which means that the free payload concentration, even after the cycling, is so minimal that it could not cause significant liver damage to a human body. As you all know, or you might know, the liver is really the only target organ for the free payload because only the liver cells have the specific transporter to pick up α-amanitin. As I just said, the α-amanitin half-life is so short that it is washed away from the circulation really fast and goes to the urine. Next question is, how many patients are in cohort nine? How many of them are post-BCMA and how many show a 17p deletion? Yeah, thank you, thank you so much. Unfortunately, because cohort nine is still ongoing, we are not able to release any data as of today on cohort nine. Stay tuned. We will release as soon as possible. We will release data on cohort nine, hopefully really soon. Okay. Next question is, why is the complete response patient in the fifth cohort no longer on treatment? The patient experienced, after two years of treatment, the patient was in two years, in the study. After two years of treatment, the patient has shown signs of disease progression and was taken off study. Next question, P53 has also been implicated in aminotin mechanism and efficacy. Is this a consideration you will have in your clinical trial design? I think I already answered this question. This is the P53 is the 17p deletion story. We rule specifically into the 17p deletion patient. Yes, we consider this in our current trial design and further trial designs as well. Currently, there are no further questions. With this, I would like to hand back to Andreas. Thank you. Thank you so much for the excellent question. If you want to ask questions, please do not hesitate. Maybe at the end of my session and my conclusions, we can still have some time if there are any further questions coming in. On top of what Professor Raab said, I just want to really highlight the key take-home messages on our today's session and recent announcement in our clinical development. I really want to focus on the last cohort. What is the take-home message? This is the highest cohort, and the highest dose that we tested is 140 micrograms per kilogram. Having said that, just a reminder that this drug is really potent. We are in the microgram range and not in the milligram range in other ADCs. Just to keep in mind, because of the different mode of action, this is a highly potent drug. This has also been demonstrated as expected in our clinical trial. We enrolled eight patients in this cohort, from which seven is available patient. From these seven, we already saw four patients who responded to the drug. What was a really important change from the previous cohort, as you remember, as Professor Raab showed you, in the previous cohort, in the lower dose cohorts, those responses were not coming really quickly. We see a partial response in a couple of cycles and then it is deepened maybe into a more deeper response. Now we already saw patients presenting VGPR after cycle one, which was deepened in stringent complete remission after a couple of cycles. Again, please remember this is preliminary data. The study is still ongoing. These patients are still ongoing. Do not draw the conclusion that the duration of response is short because these patients are still ongoing. You know that we had a patient on a significantly lower dose who was treated for two years, with a really good and massive duration of response for this patient. This is efficacy. Efficacy results in our perspective are really excellent, outstanding, and we are really happy to share this information with you. How about the safety? I think this is again, focus on this last cohort. You see the lack of grade 3 and 4 side effects of any of the patients, especially in the first couple of cycles. Again, as Professor Raab said, please focus on the lack of ocular toxicity. As you might know, other ADCs, especially monomethyl auristatin-based ADCs, are known to have ocular toxicity or known to have caused really strong myelosuppression, not just thrombocytopenia. I'm talking about real myelosuppression, which is lymphopenias, neutropenia. This is a common side effect for these other toxin-based ADCs. This is what you don't see with aminotin. This is really because of the different mode of action, because the different mode of action ensures that the free payload does not harm the surrounding, does not harm any other cells, not capable to harm any other cells, just the liver cells, as we mentioned previously, be the who has the specific update. As we demonstrated and as I answered in the question and answers, the free payload is washed away really quickly from the circulation. In summarizing, compared, we know BCMA is a, is it, it's a crowded market. We know that BCMA, lots of drugs are available in the BCMA, CAR-Ts, bispecifics, other ADCs. All of them are excellent drugs. They are capable to induce really deep and durable responses for many of the patients. But some of them come with costs. Obviously, CAR-Ts are not really suitable to apply in the outpatient setting. This is a highly complex treatment. Bispecifics are linked with cytokine release syndrome. Also, the patient has to undergo more surveillance. As mentioned here, the T-cell exhaustion and the exhaustion of the CAR-T cells and the natural and our own T cells are a problem with these drugs. Other ADCs are more like off the shelf and with outpatient settings. The importance of the outpatient setting is that majority of the patients are still in outpatient setting, also in the US and in Europe. This is a broad applicability for an ADC is clear, for that particular reason. Do not forget the hallmark or the key to each and every patient treatment, especially early alliance treatment, is the combination. If we are able to develop a drug, which has this really mild safety profile, that we presented in the last cohort, this opens up tremendous opportunity to combine with other drugs, which means that we do not have and we do not expect to see any kind of synergistic side effects with other drugs. Because as Professor Raab just demonstrated, we had this transient thrombocytopenia, but we managed to keep it in the bay with these new treatment modalities, with the pre-medication and with the split dosing in the first cycle. Having said that, where are we going with this drug? This is really important. I think I already highlighted in the question and answer sessions. Obviously, one of the lowest hanging fruit for us is the post-BCMA field. Currently, this patient has really limited treatment option. This is one of our key strategies to establish this drug as a monotherapy in a late line setting in the post-BCMA field. Why do we think that this is feasible? First of all, we already had patients who showed response despite they were treated with BCMA drugs prior, especially that showcase patient that Professor Raab presented to you. That patient particularly had received a CAR-T cell treatment with the BCMA and achieved only a VGPR on the CAR-T cell treatment. After that, after a certain pause, was put in our clinical trial and the patient was in stringent complete remission for two years in our clinical trial, which I think is a beautiful story. The patient was, as the PI said to us, really happy with the drug, and currently, just recently, was diagnosed with disease progression after two years of treatment. Post-BCMA field is obviously one of our lowest hanging fruit, but because of the broad applicability with combination, we would like to develop this drug in combination treatment as well. One of the approaches is to go in a kind of second, third line treatment, combine this drug with an immunomodulatory drug, dexamethasone, or other combinations are also possible. This is similar to the DREAM-8 study, for example, or similarly to the DREAM-7 study, which was recently approved in Europe and also partially in the US, from GSK, really good data presented with this combination. Obviously, this is something that we want to target as well. We also do not forget the third pillar, which is the high-risk patient population. We biologically expect to see, and this was demonstrated non-clinically in several papers. I know that you most likely knew this data, that this drug should be more effective on patients who harbor the 17p deletion. This is something that you see quite often in the high-risk patient population. However, addressing this is a kind of rare mutation, which means that 10% of the newly diagnosed patients show, I think, it's not the top of my head, the most recent results, but it's enriched in the later lines. In later setups, you see more patients of this. Addressing this, if we can demonstrate in our clinical trials that we have an increased efficacy, or enhanced efficacy in this particular patient population, then we definitely will develop this drug also as a third pillar in the high-risk setup, either as a newly diagnosed heart disease or as a relapse refractory drug. Of course, this also requires, especially the newly diagnosed, that this is done in the combination setting. Regarding timelines, currently we have the phase one dose escalation and the phase two expansion, early expansion, ongoing. We plan to finalize this study in the next fiscal year. After that, when we have the results ready, we would like to initiate the already announced single agent trial, pivotal single agent trial, which is capable to, or has the premise or the potential to apply for an accelerated approval. To convert this accelerated approval, you need a phase three trial. We already plan to do this phase three trial in earlier lines of treatment with a combination treatment. Of course, this needs to have as a prerequisite a combination safety study, which we can do in the next couple of years. We can convert the accelerated or conditional approval to full approval already with a combination treatment and addressing two huge markets in the myeloma field, as you can see. We can also, as a lifecycle management on the later development, explore other combination, other lines of treatment. Nevertheless, at the end, we would like to address the high-risk patient population also in the newly diagnosed and in the relapse setting. This aminotin-based ADCs, ATACs as we call them, they really show these responses. Currently the dose escalation is ongoing. We have not reached the MTD yet. We are seeking to reach this MTD as soon as possible. That is why we highlighted this last cohort, because we think that this is clearly below the maximum tolerated dose. We have not seen any grade three, four, acute toxicity for this patient population. We have really provided clinical evidence that aminotin works as a platform, aminotin works, and has a therapeutic window because we have responders on a dose level where you do not see toxicities, untolerable toxicities, but you see responses developing in this patient. It has a really good safety for it. One of our investigators told me recently that the patients were really happy with this drug. This is one of the most mildest drug ever, because they don't have, they don't suffer. Most of the patient, which we saw this thrombocytopenia, they don't feel anything. They are not feeling sick, they are not losing hair, they are not feeling nausea, fatigue, or any kind of, really typical, or cytokine release syndrome or any itches, rashes, nothing. There is no ocular toxicity, no real renal toxicity. Myelosuppression is really just limited to this thrombocytopenia, but there is no real myelosuppression in the terms of eliminating precursor cells or, or stem cells. We don't have, and on the tested doses, we don't have definitive liver damage. We do see elevations of liver function tests, but those are not fulfilling the criteria of definitive liver damage. Those lab findings are just transients. This is really demonstrating that we can overcome resistance, overcome resistance from prior BCMA-targeted drugs or overcome resistance to other prior multiple myeloma drugs. All of our patients who are in the study are heavily pre-treated. This is a last resort type of trial. Whoever we enroll in the study has really limited treatment option in the particular countries, which includes the US and Germany, where quite a few really powerful drugs are available. We are still able to achieve really good responses in this really heavily pre-treated designation. I know it's already spoiled in the questions, but I'm happy to announce that we just received the fast track designation from FDA recently. To put it into perspective, why is it important? This is important because it's an external validation. The US FDA validated our clinical results and granted us the fast track designation, which opens up for us more opportunities when we talk about later lines of development of this drug. I just can echo myself that we have not reached the MTD yet. We hope that we can reach it soon. This drug has a really good therapeutic potential. We expect to have the recommended phase 2 dose early 2026, so in the, so to say, in the upcoming month. Stay tuned for the next result. Looking a little bit broader and behind that, obviously we were talking about only on myeloma patients, but these clinical results really have an outlook on other similar ADCs because HDP-101 is not our single molecule. We already have HDP-102 in the clinic. We tested the first dose cohort, and that dose cohort was without the DLT, and in CD37 positive non-Hodgkin lymphoma. We also have a prostate cancer program, which can be developed, targeting PSMA, which is also a quite high unmet medical need for those patients to develop a mild drug as maybe similar to my drug as HDP-101 for a really, not so easy patient population at prostate cancer who are really elderly and frail, for that. We have a portfolio including many other drugs like a gastric and colorectal cancer drug. We also have a few collaborations with other persons like Takeda. With that, I will conclude my summary and I'm looking to the question and answer, and I ask our colleagues, do we have any further questions? Yes, we got a couple more questions. The first one is, why did treatment get stopped for the successfully responding patients if there were no harmful side effects and they did not die? Wouldn't progression be a reason to increase a successful treatment instead of just stopping it? Most of the patients who respond to the drug are treated until disease progression or there are some cases where, and this is individual decisions, where patients make the selection not to continue a clinical trial, but this is something that we cannot control. The majority of those patients are treated until disease progression. Can you give an update on how you think about outlicensing or partnering HDP-101? What data or de-risking of HDP-101 would you need to show to qualify for an attractive deal? When do you consider it is a good timing for partnering? Really excellent question. I will redirect this question to our business development expert. I'm not really the expert. I'm the clinical expert in the community and we will get back to you with the answer. Next question is, can you provide an estimate on the cost for the planned clinical trials? Do you have sufficient resources to conduct all planned clinical trials in parallel or would you need to prioritize? As you might already know from the recent announcement that we had to prioritize some tasks, but what I can ensure you is that the HDP-101 clinical trial is our utmost priority to complete this study, which would enable us also to do the next steps and create the financial means for the next steps of development. When do you expect your Chinese partner, Huadong, to start its registered HDP-101 phase two in China? Which data is Huadong looking for before making that decision? Thank you so much. I can't share the details, but really soon. Preparations are ongoing. There are no further questions at this time. Thank you so much. Having said that, thank you all for participating in this excellent webinar. Thank you especially for your questions. Thank you, Professor Raab, for the excellent summary. Please stay tuned and look forward to our next release. I think we all agree that these data are really demonstrating that HDP-101 development is progressing in the right direction. Hopefully we can give you more updates on the ongoing cohort nine soon with the development. With that, I conclude this webinar.