Vivoryon Therapeutics N.V. (VVY) Earnings Call Transcript & Summary

Good day, ladies and gentlemen, and welcome to the Vivoryon Therapeutics Half Year Results for 2022. Information in today's conference is being recorded. And at this time, I will turn the call over to your host today, Ms. Manuela Bader. Please go ahead, ma'am.

Thank you, George. Good afternoon, and thank you for joining us today for Vivoryon's conference call to discuss the company's first half 2022 results and operational progress today, including details on the [indiscernible] we announced earlier this morning. This morning, Vivoryon issued a press release reporting its first half 2022 results. This is posted on the company's website at www.vivoryon.com. On the call with me today are Uli Dauer, our Chief Executive Officer of Vivoryon; and Florian Schmid, our Chief Financial Officer. Also with us on today's call and available for questions is Michael Schaeffer, our Chief Business Officer. We will begin today's call with opening remarks from Uli on Vivoryon's approach to overcoming the challenges of AD drug development, our strategic focus and progress and then Florian will review the financial results for the first half of 2022. Following the prepared remarks, we will hold the Q&A session. Before we start, I would like to remind you that during this conference call, we will present and discuss certain forward-looking statements concerning the development of the Vivoryon Therapeutics core technologies, the progress of its current research and development programs and the initiation of additional programs. Should actual results differ from the company's assumptions, ensuing actions may differ from those anticipated. You are therefore cautioned not to place undue reliance on such forward looking statements, which speaks only of the date hereof. With that, I will now turn the call over to Uli.

Thank you. To contextualize the key updates for the first half of 2022, I'd like to start off by highlighting Vivoryon's approach and how it differentiates from all others in the field. More than 50 million people worldwide are living with Alzheimer's disease and dementia, currently without a chance of being cured. The devastating reality, this disease affects not only the patients themselves, but also places a heavy burden on all families, caregivers and physicians. Last year, aducanumab was approved in the U.S. as the first potentially disease-modifying treatment for Alzheimer's disease. But aducanumab is currently not broadly available to patients outside of the clinical study setting. This approval after nearly 20 years of disappointments in the space was an important signal to the community and the markets. Nevertheless, the uncertainties remaining around the potential regulatory path to approval for other Abeta-antibody-based approaches have considerably dampened the overall enthusiasm. Unfortunately, an extremely high unmet medical need remains for safe, effective and widely available treatment options. The last couple of days have seen a surge of excitement in the AD community, based on the positive data published by Eisai and Biogen for Lecanemab, an investigation and anti-amyloid-beta protofibril antibody. According to today's press release, this -- according to Tuesday's press release, I'm sorry, the Phase III confirmatory Clarity Alzheimer study met primary and secondary endpoints and the incidence profile of amyloid-related imaging abnormalities, or ARIA, had adverse events associated with anti-amyloid antibodies was recorded to be within the development expectations. These results are obviously very encouraging for all those affected by Alzheimer's disease and for the community as a whole as we will help the field to better understand the relevant factors in Alzheimer's disease drug development and further enhance the overall knowledge base in Alzheimer's disease. And I'll talk a bit about more why we at Vivoryon feel that these results are particularly interesting. First, I'd like to explain why independent of the results from other programs in Alzheimer's disease, we believe that with varoglutamstat, we have a unique, differentiated approach to address Alzheimer's disease and, therefore, have a great chance to add a different [fibrillary] [indiscernible] to the emerging [fibrillary] landscape. At Vivoryon, we are fully committed to making a real difference to all of the people affected by this merciless disease. Our approach is to treating Alzheimer's disease or our approach to treating Alzheimer's disease is very different from antibody-based approaches and from those that focus solely on the amyloid aspect of the disease. I'd like to briefly share with you why this is the case and why we believe that this will allow us to become an important part of the solution to end the Alzheimer's crisis. We are specialized in developing medicines to block the misguided activity of certain enzymes that either cause diseases or allow them to progress. Our most advanced medicinal development, varoglutamstat, is a small molecule, designed to overcome the chances of Alzheimer's disease drug development. Varoglutamstat is in clinical Phase IIb development, and it has a unique dual mode of action that is truly differentiated from the other approaches in clinical development, which is shown in the graphic on the right-hand side. Firstly, as you can see in pink on the left, varoglutamstat blocks the enzyme glutaminyl cyclase or QPCT for short, and this prevents formation of neurotoxic N3pE amyloid, a toxic Abeta variant shown to play an important role in the development and progression of Alzheimer's disease. Importantly, this happens way upstream of other approaches, which means that varoglutamstat can also have an impact on other downstream pathologies such as tau pathology, neuroinflammation and synaptic impairment. There's a second important pathway on which varoglutamstat acts, which is shown here on the right side in dark purple. Q is iso form of variation of glutaminyl cyclase called QPCTL, upregulates or boosts the pro-inflammatory signaling molecule CCL2 by turning it into pE CCL2. So by blocking QPCTL, we are able to reduce neuroinflammation. Moreover, CCL2 is also a promoter of the tau pathology, meaning that we can also address this pathology via both elements of varoglutamstats mode of action. Varoglutamstat is modulating all important pathological formats of Alzheimer's disease, a beta pathology, neuroinflammation, tau pathology and therefore, can protect synaptic function. Now coming back to lecanemab. According to its developers, the antibody is designed to bind to soluble Abeta aggregates rather than only larger insoluble aggregates or plaques and can, therefore, be considered a bit further upstream than, for example, aducanumab. But what I want to stress here is varoglutamstat stat is the first small molecule, and to our knowledge, the only project in clinical development selectively targeting the de novo production of neurotoxic N3pE amyloid. So we have the opportunity at our hands to attack Alzheimer's disease pathology even further upstream than lecanemab. And there's another huge benefit of varoglutamstat being a small molecule. With antibody-based therapies in Alzheimer's disease, safety of the patient is one of the main concerns. We've already characterized varoglutamstat broadly, and I'll show you in a moment what we've seen there in terms of safety and tolerability. Another key advantage of our approach is that while many drugs in development in Alzheimer's disease are antibodies that has to be injected or infused, we focus on small molecule medicines. So varoglutamstat can be very conveniently administered as an oral pill. We carefully designed our development program with a clear regulatory path in mind towards bringing it to patients in need as soon as possible. And our development strategy is rooted in promising Phase I and Phase IIa results. The varoglutamstat was well tolerated and showed statistically significant changes from baseline in working memory-related parameters after only 3 months of treatment in patients suffering from Alzheimer's disease. Before we dive deeper in our clinical development highlights and how this fits into our overall development strategy, I'd like to start with a number of important corporate developments. Building on the progress we made throughout 2021 and 2022 year-to-date and despite the overall market conditions our industry has been facing over the last year, we were able to successfully complete 2 substantial financing rounds. In April 2022, we were able to successfully raise EUR 21 million in a private placement supported by a number of high-quality institutional investors from Europe and the U.S. as well as executives and nonexecutive members of our own Board. And as announced earlier today by means of a press release, we have entered into another private placement of EUR 15 million, supported by our long-standing investor, Claus Christiansen, and our new investors, KKR Dawn Aggregator, a platform controlled by affiliates of KKR, a leading global investment firm. The investment agreement includes an additional option for the investors to place up to another EUR 15 million during a period ending 12 months after the date of the approval of an EU recovery prospectus or 3 months after the achievement date of a defined clinical milestone, whichever is latest. Having secured these significant private placements will enable us to continue to follow our carefully crafted development strategy. We warmly welcome our new investors, Dawn Biopharma and are very grateful to them and to our long-standing investor Claus Christiansen as well as those shareholders participating in our April financing round, for their support through the upcoming clinical milestones. On the leadership side, I'd like to highlight that we expanded and diversified our team with the appointment of Dr. Claudia Riedl and Samir Shah, MD, as Non-Executive Directors of our Board. In addition to our own efforts, the regulatory achievements of our Chinese partner, Simcere, enabling near-term clinical development in China, broaden the tremendous opportunity for us to make varoglutamstat available to as many patients who need as possible. Moving on to our clinical portfolio highlights. 2022 year-to-date was marked by decisive progress in the development of varoglutamstat in Alzheimer's disease, which accumulated several data presentations at the prestigious AAIC conference in San Diego in July and August, and there are a number of highlights I'd like to share with you today. Firstly, we have been able to further derisk clinical development of varoglutamstat with extremely encouraging safety results from our VIVIAD Phase IIb study where we completed the parallel group, dose finding part, and the independent Data Safety Monitoring Board selected the highest dose investigated, 600-milligram twice daily as final dose in the second part of this study. At the same time, further substantiating the rationale for evaluating varoglutamstat in combination with monoclonal antibodies to treat Alzheimer's disease. Also at AAIC 2022, we presented preclinical data underscoring the unique mode of action or the unique potential of our N3pE amyloid-targeting therapeutic strategy in both mono- and combination therapy settings in Alzheimer's disease. The data show that a combination treatment of aducanumab and varoglutamstat achieved additive effect on Abeta pathology, indicating feasibility of dose reduction to improve safety of Abeta antibody-based Alzheimer's disease treatments. This demonstrates the potential benefit of a combination therapy designed to simultaneously make use of 2 different independent molecular N3pE related mode of action, namely small molecule-based reduction of N3pE amyloid by QPCT and QPCTL inhibition and clearing existing Abeta deposits through anti-N3pE Abeta immunotherapy. Additionally, together with our collaboration partners, we published data at AAIC 2022 from the murine analog of PBD-C06, highlighting the differentiated safety profile with other anti-Abeta antibodies that N3pE amyloid-lowering concentrations. Together, previous published data showing that varoglutamstat in combination with our own N3pE amyloid specific antibody, PBD-C06 has an additive effect on reducing brain Abeta pathology in transgenic mice. The data set presented at AAIC 2022 adds to the overall treatment data package, enabling us to explore the full potential for varoglutamstat application in a variety of therapeutic settings. While we're currently focusing on developing varoglutamstat as a monotherapy, we see great potential in further investigating this approach in the future. Our second ongoing clinical study, VIVA-MIND in the U.S., the Phase IIa/b study varoglutamstat is actively enrolling patients. There are currently 14 sites open, and the study is on track for interim futility analysis planned for the first half of 2023. And I'll give you a bit more detail on our ongoing Phase II studies now. What's important to understand here is that carefully crafted study design, we were able to achieve improved tolerability varoglutamstat compared to the prior Phase IIa study, our SAPHIR study. SAPHIR reported encouraging first evidence of the disease-modifying activity of varoglutamstat, most importantly, with statistically significant changes from baseline in working memory as an important cognition visibility after only 3 months of treatment. While varoglutamstat was generally well tolerated, a maximum tolerated dose was reached in the study at 800 milligrams daily. We were extremely happy to report to media that we were able to reduce this discontinuation rate from 33% in SAPHIR to 1.1% VIVIAD. Now from our extensive PK/PD data, we know that 600 milligrams twice daily results in a high target engagement. We are talking about 87% here. So we are able to achieve improved tolerability for varoglutamstat without significantly sacrificing target engagement. For VIVIAD, following the data safety monitoring Board decision to move forward with 600 milligrams twice a day for the second part of the study, we are well on track with 22 active sites in 5 countries, gearing up to final readout in the second half of 2023. I'm truly grateful to everyone involved in the study for their outstanding efforts to meet the challenges all clinical studies around the world have faced over the past 2 years. And the same goes for VIVA-MIND, the U.S. study we initiated in September last year, which is run by the ADCS and supported by an NIH plant. Despite the pandemic and also weather-related challenges in the U.S. during the winter, the study is open with 14 active sites and randomizing and treating patients in the ongoing Phase IIa part of the study. VIVA-MIND is on track for interim futility analysis in the first half of 2023. If predefined criteria are fulfilled in this analysis, the trial will pass the stage gate into the Phase IIb part. Before we move to the financials, I would like to point out where these great results and upcoming milestones fit into overall in our overall development. I will go into detail at this stage other than stating that we are following the diligently designed development strategy without cutting corners. We've completed preclinical work showing the effect of QPCT blocking on cognition in well-known Alzheimer's disease mouse models. In the completed Phase I clinical study, we've shown that varoglutamstat is well tolerated, and we also got important information on dose response and target occupancy. And as mentioned before, our first trial for patients with Alzheimer's disease, the Phase IIa SAPHIR study, met not only the primary objectives of obtaining important safety information. but we were also able to show first evidence of the disease-modifying activity of varoglutamstat, most importantly, with statistically significant changes from baseline in working memory as an important customer disability after only 3 months of treatment. These Phase IIa results guided the design of our ongoing European Phase IIb study did. Both our VIVA-MIND U.S. and VIVIAD EU studies are designed to align with the dropped guideline, which supported by the more frequent interactions we can benefit from due to our fastrack designation, may provide further regulatory opportunities such as breaking designation and accelerated approval provided all further relevant criteria in the context of our studies and the outcome of our [indiscernible]. So in summary, our overall data set is intended to support a clear path to approval for varoglutamstat. And with that, I'd like to hand over to Florian to review our financial results. Florian?

Thank you, Uli. In the first 2 quarters of 2022, our research and development expenses amounted to EUR 11.1 million versus EUR 9.5 million in 2021. This increase was mainly driven by EUR 1.7 million higher expenses related to our clinical trial, VIVIAD, which has advanced significantly compared to the 6 months ended June 30, 2021. When looking at the general and administrative expenses, we have reported a cost level that is similar to the 6 months ended in June 30 in 2021 of EUR 2.3 million. The reason for that is that higher expenses for share-based payments worth EUR 0.3 million were fully compensated by EUR 0.3 million lower expenses for media and consulting services. The company did not generate any licensing revenues in the 6 months ended June 30. And as in previous periods, our finance result was preeminently driven by the FX results on U.S. dollar cash or receivables, liabilities denominated in U.S. dollars. The main receivables and liabilities denominated in U.S. dollars results from the licensing deal with our partner [indiscernible] that was executed in the second half of 2021. For the first time, we see -- for the first time, we have reported income tax expense, consisting exclusively of deferred tax expenses. The reason for that is a very narrow definition in IAS 12 on how existing loss carry forwards may be recognized. The result was a temporary excess of deferred tax liabilities. The increase of deferred tax liability excess in the 6 months ended June 30, 2021, by EUR 89,000 was recognized as a tax expense in the same period. All this together resulted in a net loss of EUR 12.6 million or EUR 0.60 per share for the first 6 months of 2022 compared to EUR 11.7 million or 0.58 per share in the half -- in the first half of 2021. When we move to the next slide, I would like to highlight only some of the KPIs. The company held EUR 24.4 million in cash and cash equivalents as of June 30, 2021, compared to EUR 14.7 million as of December 31, 2021. If you look at equity or the number of shares, you can see that we issued 2 million registered shares at the beginning of April 2022. On April 1, 2022, the company completed a private placement by the way of accelerating [ book reading ] at an offering price of EUR 10.5 per share. The new shares from the capital increase represented 10% of Vivoryon's existing share capital. The company's issued share capital, therefore, has increased to EUR 22,050,482 . Our negative cash flows from operating activities was EUR 10.2 million for the 6 months ended June 30, 2022 compared to EUR 6.1 million in the 6 months ended June 30, 2021. The increase in negative cash flows by EUR 4.2 million was mainly due to EUR 4.7 million higher decrease of accounts payable in the 6 months ended June 30, 2022 compared to the 6 months ended June 30, 2021. While the investing cash flows remained virtually unchanged, our cash flow from financing activities was EUR 19.6 million for the 6 months ended June 30, 2022, compared to cash used in financing activities of EUR 0.5 million in the 6 months ended June 30, 2021. The change mainly relates to the completion of the beforementioned private placement on April 1, 2022. The gross proceeds of that offering were EUR 21 million and the transaction costs amounted to [indiscernible]. The above described cash flows resulted in our cash and cash equivalents position of EUR 24,400,000 at June 30, 2021. And with that overview, I would like to turn the call back to Uli for brief concluding remarks.

Thanks, everyone, for joining us today. I'd like to conclude by emphasizing that all data generates by ourselves and published by others to date support our unique approach, which is to target N3pE amyloid, the molecule, we believe, to be the main driver of Alzheimer's disease. Thereby, we have the opportunity to address all pathological hallmarks of the disease, namely modulating Abeta pathology through preventing the formation of N3pE amyloid, attenuating neuroinflammation by destabilizing the pro-inflammatory signaling molecule CCL2 and modulating N3pE and CCL2 dependent tau pathology and synaptic impairment. In addition, I would like to reiterate that varoglutamstat is an orally available small molecule, not an antibody, coming with a high risk of [indiscernible]. And I would, once again, like to thank our shareholders, many of which have been following our progress for many years now for their continued support and welcome our new shareholders. The data set generated during the reporting period and year-to-date have sparked excitement within the medical community and beyond, and further substantiate our commitment to making a difference to all those affected by Alzheimer's disease. We look forward to keeping you all updated on our progress, and we'll now open the call to take questions. Thank you. George?

[Operator Instructions] Today's first question is coming from Mr. Joseph Hedden calling from Rx Securities..

First of all, congratulations on a great progress, really fantastic in this environment, as we know. Linked to that fund raise, for the second EUR 15 million, one of the conditions was linked to a clinical milestone, which -- the clinical milestone or the release the prospectus of a [indiscernible] -- could you confirm what the clinical milestone is, by any chance?

Joseph, first of all, welcome on our call and thanks for your congrats. Joseph, unfortunately, I can't go into a more granular level than we stated in the press release at that time.

Okay. Okay. I appreciate that. It was worth a shot. Secondly, I just wanted to ask a question about the patient characteristics of the VIVIAD and VIVA-MIND trials. So you [indiscernible] have made quite a big deal about how they have recruited quite a balanced proportion of ethnic minorities into the trial. And this was an FDA criticism of the aducanumab trial because they didn't do that very well. Is this something that you've kind of actively built into your recruitment policies as well so that you don't run into similar issues later?

Joseph, that's Michael. Nice meeting you again by phone, and thanks for the congrats also from my side. Yes, so the answer is clearly yes to that. And obviously, we are continuously work very close with ADCS. And the requirements, especially in the U.S., are familiar to us. And we have, let's say, special programs to address minorities in the U.S. So this is well reflected in our recruiting as well.

Okay. Great. And then perhaps lastly, could I just ask a conceptual question on the mechanism of action of varoglutamstat, specifically the pyroglutamate side? So we know that targeting amyloid beta with antibodies is likely to be more effective when the patient is in APOE carrier. Is that the same when you are targeting with a drug like varoglutamstat is shutting off production? Or should it should have equal efficacy regardless of APOE status?

Yes. Thank you for that question. The answer, Joseph we don't know because the population, which we had in our SAPHIR trial, in the 120-patient trial, was just too small to really have kind of decent analysis on that basis. So we just have no evidence for any kind of conclusion yet. But enrollment with respect to ApoE4 carriers is very balanced, and we certainly will see once we have the final data of [indiscernible].

We'll now move to Alexander Galitsa, coming from H&A.

A couple of questions, Please. First...

Sir, could you please speak up a little bit? Your line is very low.

Can you hear me?

Could you maybe increase your volume a bit, sir, please? Yes. Now that's better.

Okay. Apologies. So the first question is on the cash reach. Before this capital raise, the cash reach was I think at least until May 2023, which I think already reflected larger part of necessary R&D outlays. Now with this incremental EUR 15 million, you say cash reach is until -- at least until the end of 202. I would expect the cash reach to be well into 2024. So I was just wondering whether you could explain why are you being more conservative in your wording?

Well, I mean, being more on the safe side, I think it's always the better choice, but you're absolutely right. So including the proceeds from this private placement and according to current planning and estimates, we expect the existing cash and cash equivalents to be sufficient -- yes, to at least finance our activities through December 2023. And this does not include any exercise of the options to acquire additional shares, which was part of the recent transactions, nor does it reflect our options based to evaluate and pursue additional financing measures.

Okay. Understood. And then the question on KKR joining as a shareholder, given that it's obviously a U.S. company, does this bring the idea of a potential U.S. listing, further down the road, back on the agenda?

Well, I think we never kind of have given up on the idea to also expose ourselves to the U.S. market. However, currently, we don't feel that it's the right point in time. And I mean an investor like -- the funds which invested out of KKR is certainly a supporting element for whatever we might plan in the future. But again, we haven't been specific on any time lines and plans as to a potential asset listing.

Okay. Fair enough. And then maybe on the -- on your preclinical antibody. So quite clearly, Lecanemab data have really sparked interest in those class of drugs. So I was just wondering whether this changes anything in the way you're thinking about opportunities for your own preclinical assets?

I mean, we always believed in our antibody being really interesting and a good one. So -- but of course, I mean, we see, as I say, logically starting interest in that area. And I mean, does in the end we think, could only help the case. As you know, the antibody is still in preclinical state, but we continue to develop that. And -- yes, try, of course, always to exploit the situation as it unfolds.

And just to clarify maybe on that, so plan A would be, I guess, presumably not to really go into more expensive trials with this antibody, but the -- is the plan A then really look for a partner who might either buy it outright or join to really help financing it? Or what's the Plan A here?

Alex, this is Uli again. It's clearly an opportunity to enter into early partnership, which we essentially already did in the context of this sincere partnership. So they are already taking care of the antibody. So there's, of course, ambitious, and I think it's a great asset to progress development mainly through our partnership with Simcere or potential future partnerships in rest of those as to speak.

Understood. And the very last one is with respect to Simcere. Do you know what their plan is in terms of -- I mean, they licensed in 2 assets, right? A small molecule as well as the preclinical antibody. Do they simultaneously pursue both strategies sort of in the development? Or are they now mostly focused on the small molecule? That's the first question. And the second question to it is whether you think or have indication that they're still able to start Phase I this year?

So about the first question, I mean, it comes from the nature of the deal we made with Simcere you remember, they require this option to develop the antibody. So you might assume that, of course, for the time being, the development of varoglutamstat or small molecule is a little bit prioritized over that. However, as we say. So they're continuously working on the antibody as well. And in terms of when the clinical phase is really starting, I cannot really comment on that because this is truly in the hands of Simcere. As we indicated, the plans are ongoing in that kind of a similar changes to the work on preparing the Phase I and Phase II in China. So -- but when this is really happening is this is still within this year or at some point of time next year. And -- I cannot comment on that.

We'll now go to Andrew Oscari from -- calling from Lemanik.

A couple of questions from me. The first one, a very -- sorry, very simple question. I understood basically all the development of the success on the clinical trials that you had. My simple question is, why -- what kind of explanation do you give to the fact that at the moment we are talking about the company with a EUR 200 million market cap with this kind of potential ahead? So basically, what's missing in your view to better -- to let better understand the value inside the company of all the achievements that you have reached? This is the very simple question.

Yes. Thank you, Andrew, for joining, and thank you for your question. It's really a tough question for us to answer because we can't really explain a man dynamics on the capital market. So it's really tough for us. So the question is what can we do? And here, again, we are laser focused on increasing the value by progressing our development for Varoglutamstat. I think we have very exciting milestones upcoming. Again, to remind what we have presented in the presentation, so we expect the futility analysis of the [indiscernible] trial in the first half of next year. We expect the full data readout in the second half of next year. So there are exciting potential value inflection events ahead of us, which I would expect should impact the value perception of our company.

Okay. It's very clear. I try to better explain my question again. Apart from the recent fundraising of today and the entry of KKR, that is fantastic, fantastic news for us as shareholders, are you basically in touch or, let's say, in the radar screen of larger pharma companies that are looking at your developments in order to finalize joint ventures, agreements, whatever, now that the clinical trials, I repeat, are going much, much better compared to what were a year ago? This in order to fully exploit the value of the company. This is a -- I tried to better explain the question.

Yes, we are thanks. And I think an important component was already mentioned by us in terms of how are we appearing on the radar screen. So we have mentioned a couple of data presentations in the context of this prestigious AAIC 2022 conference, where there were a lot of attendants from the industry. And again, we believe that we sparked a lot of interest with this new data, which we have presented there. And that kind of makes us very, very optimistic here. So that will be my answer to your question,.

[Operator Instructions] We'll now go to [indiscernible], calling for [indiscernible] Asset Management.

I hope you can hear me, I'm calling from overseas. My question is the following. We are loyal shareholders. We have also been in the capital increase only 5 months ago at EUR 10.50 a share. And we're a bit surprised that we were not offered any dilution protection in the current round at EUR 7.30, which is 30% below the EUR 10.50 in April. Are you planning any measures to at least protect that group of shareholders that were part of the April capital increase to protect them from dilution in this round?

Yes. I mean, we were pretty transparent, I think, for the terms of this transaction and -- the question, if I read right to why do we choose for this type of deal. And I mean that's always a careful evaluation of different options to ensure that the company is well funded and able to deliver on strategic objectives. And yes, thereby also generating stakeholder value. And yes, let me make it very clear that our commitment is, first and foremost, our patients. So Varoglutamstat mode of action which, to our knowledge, allows the intervention upstream of all other approaches currently in clinical development, we really have a unique chance at our hand. So we believe being able to progress our tend studies and providing our study drug to all those participating in VIVIAD -- VIVIAD and VIVA-MIND is of utmost important center, that's kind of still the parameters for our decision here.

I don't understand. what is the downside of offering shareholders, which were giving you money in April at EUR 10.50. What is your downside in offering them the same terms I can't see any downside for the company?

So the -- particularly terms we were discussing here with the management and the Board, in our view, were necessary to attract such kind of investors with whom we are talking about. So that's the basic answer to your question here.

So they were asking you not to let any other shareholder...

Does that answer your question, sir?

They were asking you not let old shareholders participate in this round. Is that the way I have to understand this?

It was a deal which we made in alignment with the partners. So it was a mutual decision to structure the deal to make it -- yes, win-win for both sides here.

[Operator Instructions] We'll now move on to our next question coming from Chris Redhead calling from goetzpartners.

Yes, sorry, I got booted out of the call for a little while, so I hope I haven't -- ask something that's already been asked. Just in terms of this -- just kind of interested, very interested in the combination therapies that you talked about. As I understand, the antibody you've done those studies in is similar to the Lilly one, is that the case? It's a N3pE antibodies, is that right?

That's correct. So our own antibody basically has the same target as the Lilly antibody and as our small molecule in the end as well. So N3pE, that's correct. However, our antibody is kind of modified. I mean you know that the antibodies have the this part, which is important for recognizing the antigen and there actually the other part, which is called Fc domain or so where -- which has some effect of functions. And within this domain we have put in a specific point mutation, which then leads in the end to having the complements to not activated by this antibody, so is what other embodies would do, which don't bear this point mutation, which is [indiscernible] protected also by us. And this leads to a much less or much lower immunogenicity profile of our antibodies. So leading to, again, presumably less antidrug antibodies, but also less areas. So it's a modified N3pE specific antibody we are developing here.

Right. Actually, so it's going to kind of getting at was -- you've got this very interesting data with Lecanemab which it's -- you're now looking at the soluble -- do you have any sense of how much Lecanemab is taking out the N3pE. I don't know whether that -- if there's any data on that. because it's kind of interesting that, that antibody works and actually the combination of your product would that maybe have an even broader effect given that it's a different -- that the antibodies has a different target. I just sort of kind of thinking about the different combinations, all these different combinations that you can sit in the middle of this, essentially?

That's definitely the case. So what we're assuming -- I mean, you know we have published this data with our antibody. We have published data with aducanumab combination at the AAIC. And -- yes, you might assume that we're looking into other antibodies as well, but there's no data I can report to you now at this -- Uli wants also to add here.

Yes but adding or answering your question, so how much of potential N3pE would Lecanemab capture. I mean we can only speculate. But what we believe is that in soluble aggregates, the toxic potential of N3pE according to our knowledge and also other publications, much higher than in the soluble plaque. And this is a key differentiating element of Lecanemab. And that's why we are saying, obviously, it shows that being more upstream in the aggregation cascade of Abeta seems to be a successful strategy. And we are even more upstream. So we are even preventing the formation of N3pE and not taking it out once it's established. So that is the kind of an exciting fact that the...

It's a confirmation. That's kind of what I was kind of thinking about was that actually the Canada is, by its nature, also kind of not specifically targeting, but is taking out the N3pE in a much larger way than some of the other antibodies, right? Okay, that's so it's actually kind of confirmatory in that sense that the N3pE really is the target -- or is -- has the potential that we all hope for?

Yes, absolutely. So we see that as an endorsement of this of is absolutely.

The other sort of other quick question that I mean to ask sometimes when you're doing your drug is oral, did that help with process because presumably you could -- the patients didn't have -- didn't have to go into a hospital presumably to get there necessarily to get their infusions and things. Is that the case that you could more -- sorry.

Yes, I mean, absolutely. And in 2 ways, so you are right. So they have to go into the hospital to get their infusion. And secondly, and that is a requirement still for aducanumab, which is a group, and we curious to see how that will play out with Lecanemab, but patients obviously have to be very closely monitored towards the risk of developing ARIAs. And that also makes the kind of therapies quite expensive and also quite -- yes, unconvenient for patients. So we see absolutely these 2 advantages. So we haven't seen any ARIA event in our interim data in VIVIAD. And -- yes, we have an oral pill, which can be taken at home and conveniently.

I want to add to that, Chris. Chris, I just think while everybody can maybe just think about himself in that regard. So as the question is very simple, whether you want to go with Lecanemab. It's a [indiscernible] even biweekly, every 2 weeks or at least with other antibodies every 4 weeks to the clinic and sitting there or being there basically half a day because as lysis, you need to be monitored versus, yes, just taking a couple of pills in the morning and in the evening. So I mean that, of course, we think that's kind of a great advantage.

Yes. So huge advantage, particularly in this patient population in an elderly patient population, which we know are, in any case, susceptible to these kinds of infections and at any stage, you want to keep them out of the hospital, right?

Yes. Yes.

As we have no further questions, I'd like to turn the call back over to Mr. Uli Dauer for any additional or closing remarks.

Yes. Thanks, George, and thanks, everybody, for joining us at this very exciting time for us. And -- yes, we really look forward to continue to update you and to welcome you in our next call. Thanks very much, everybody. Bye-bye, and have a nice weekend.

Thank you, sir. Ladies and gentlemen, that will conclude today conference. Thank you for your attendance. You may now disconnect. Have a good day, and goodbye.