Ladies and gentlemen, welcome to the AC Immune Conference Call, December 2025, and live webcast. I am Moira, the call's operator. I would like to remind you that all participants will be in listen-only mode and the conference has been recorded. The presentation will be followed by a Q&A session. You can register for questions at any time by pressing Star and 1 on your telephone. Webcast viewers may submit their questions in writing via the relevant field. For operator assistance, please press Star and 0. The conference must not be recorded for publication or broadcast. At this time, it's my pleasure to hand over to Gary Wanders, SVP, Investor Relations and Communications. Please go ahead.
Thank you, and thank you to everyone for joining our call today to discuss the positive interim results from part one of our vaccine phase two trial evaluating our anti-alpha-synuclein active immunotherapy, ACI-7104, in early Parkinson's disease patients that we announced a couple of hours ago. With me today, we have Andrea Pfeifer, CEO; Günther Staffler, our EVP of Development; and Chris Roberts, our CFO from AC Immune, and as well, we have joining externally, Professor Werner Poewe. He is Emeritus Professor of Neurology at the Medical University of Innsbruck. At the end of our prepared remarks and invited comments from Professor Poewe, we will open the call to take your questions, so AC Immune shares, as you know, are traded on the NASDAQ stock exchange, and I'd like to draw your attention to this particular disclaimer about forward-looking statements.
And with that, I will hand over to our CEO, Andrea. Please go ahead.
Thanks, Gary, and a warm welcome from me as well. We are delighted to present this data from our vaccine phase 2 clinical trial on our Parkinson's active immunotherapy. But before we go into these very interesting results, I would like to say a few points about AC Immune. AC Immune has a very focused pipeline with multiple late-stage programs, some of them are unpartnered. Our key differentiation is our approach to precision prevention in neurodegeneration and our leadership in active immunotherapy, and one of the products you will have more information about today. Our pipeline was fully built on our two technology platforms: the SupraAntigen technology platform and the Morphomere technology platform, and these have been validated through multiple clinical candidates as well as through multiple partnerships.
Our partner programs have generated more than CHF 450 million of partnering payments, and they have a potential to generate an additional over CHF 4 billion of milestone payments plus royalties. Importantly, our cash balance finances us until the end of Q3 2027 to reach key inflection points in our pipeline. Our pipeline includes three programs in phase two development and one PET imaging diagnostic in phase three. Our lead superantigen active immunotherapy against tau and ibetta have both received fast-track designation, as you can see from the first two bars, and are being developed in collaboration with our partners, G&J and Takeda, respectively. This clearly underscores AC Immune's leadership in neurodegeneration active immunotherapy. We are successfully pursuing complementary modalities with our small molecule programs, such as our tau Morphomer, palbratiflilin, and additional preclinical assets against alpha-synuclein and the NRP-free inflammasome.
We believe it is critical to intervene in the cellular, intercellular pathologies. The next slide shows you the focused value drivers. These are programs that have the potential to generate tremendous value for AC Immune. The two first are active immunotherapies, already mentioned in Alzheimer's disease, focused against targeting phospho-tau and amyloid-beta. The third one, ACI-7104 active immunotherapy, targets alpha-synuclein and PD in phase 2 development and is wholly owned by AC Immune and offers significant opportunities, as we believe, in the future. This is the focus of our news today, which we will get into in more detail shortly. The fourth pillar focuses on the intercellular targeting and offers the possibility either of individual small molecule drug products or combinations with our active immunotherapies.
Today's announcement is the latest example of a strong value-generating innovation, and I would now like to hand over to Günther Staffler, our Executive Vice President of Development, to share the details of his interim analysis.
Okay, thank you very much, Andrea. So, as you will see, the compound ACI-7104 was designed to elicit an antibody response in humans that specifically binds to aggregated species of alpha-synuclein. And we all know that these aggregated species of alpha-synuclein contribute to the pathogenesis of Parkinson's disease. Now, Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease, but is currently the fastest growing neurological disease and affects about 1% of the population over 65 years. Most of the causes, or most of the cases, are so-called idiopathic cases, which means the cause is unknown, and just about 5%-10% of the cases can be attributed to a genetic mutation.
Now, focusing on the cellular level, Parkinson's disease is mainly characterized by the loss of dopaminergic neurons in the substantia nigra, and this loss in these neurons then leads to all the symptoms listed here in this slide. The loss of neurons is also accompanied by the formation of pathological inclusions, so-called Lewy bodies, which can be seen on the right side of this graph. And the main component of the Lewy bodies is the protein alpha-synuclein. Now, when we look to the next slide, under healthy conditions, alpha-synuclein adopts an unfolded or a coiled-shaped alpha-helical structure. And for some reasons which are not fully understood yet, alpha-synuclein can misfold, and this leads to aggregation of the protein. And this misfolding and aggregation are the molecular basis for alpha-synucleinopathies, including Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy.
The aggregated species of alpha-synuclein have been shown to interfere with synaptic function, to be toxic to neurons, and, as shown here, to be released into the extracellular space where they can spread to neighboring cells, and this seeding and spreading of alpha-synuclein are the potential drivers of disease progression. Therefore, inhibiting spreading and the uptake of aggregated species of alpha-synuclein is expected to inhibit downstream neurodegeneration and progression of the disease, so to go for a disease modification. As I mentioned at the beginning, ACI-7104 was designed to elicit an antibody response against this toxic alpha-synuclein species. The candidate delivers the clinically validated PDA1 peptide, which is a modified, optimized version of the native alpha-synuclein to elicit a target-specific antibody response. In phase one trials and data are published in Lancet Neurology, the PDA1 compound was safe and well tolerated over a period of more than 3.5 years.
It also showed the capacity to induce a strong and boostable antibody response specific for alpha-synuclein. The ACI-7104 compound is an optimized formulation that couples this optimized antigenic peptide sequences to a carrier protein, which delivers target-unrelated T cell help. Now, the compound is expected to deliver all the key outcomes listed on the right side, which is immunogenicity, target specificity, selectivity for aggregated alpha-synuclein to induce a sustained and boostable antibody response with evidence of memory B cell formation. If we now go to the next slide, today we report interim results from part one of the vaccine study, our ongoing adaptive placebo-controlled and biomarker-based phase two study in patients with early idiopathic Parkinson's disease. Now, the vaccine, as shown here, consists of two parts with a seamless transition. In both parts, the treatment period lasts for 18 months, with a follow-up period of additional six months.
Part one now focuses mainly on safety and tolerability, as well as key immunogenicity measures. Furthermore, it focuses on pharmacodynamics and biomarker measures of alpha-synuclein, and interim analysis also includes measures for clinical readouts. Going to the next slide. Now, here on this slide, you can see the inclusion criteria and exclusion criteria for this study. Now, participants are aged between 40 and 75, with a diagnosis of clinically established early Parkinson's disease as confirmed by DaT-SPECT analysis. Early PD means it must be two years or less from the onset of motor symptoms, and participants must be stage one or two on the Hoehn and Yahr scale. We have recruited a total number of 34 subjects in part one, and data analysis, and this is important, which are carried out at week 50 and week 76, are not powered for comparison between the active treatment and the placebo arm.
Now, it is important to mention now that the data we are going to share show a consistent trend across multiple biomarkers and readouts, and this is really remarkable because all those trends go in the direction of disease stabilization. On the left side now, on this slide, you can see baseline characteristics of the patients in the study. There are 22 males and 12 females with a mean age of 62 years, and patients are evenly split on the Hoehn and Yahr scale between stage one and two. On the MDS-UPDRS scale, patients generally showed mild disease scores, and the mean time since diagnosis was a bit more than 10 months, sorry. The majority of the patients, 68%, are receiving L-DOPA. On the right side now, you can see the data on safety and tolerability, and as you can see, the compound was proven safe and well tolerated.
There is a very good safety profile with no serious adverse event considered related to the study drug. The most commonly reported adverse events, as expected, are injection site reactions with 56% headache, 14%, and fatigue about 12%. Now, going to the immunogenicity results. Here, you can see how titers developed over time, and you can immediately see that in the active treated arm, which is here represented by the blue line, titers increased steadily over time, and you can see the significant increases in titers after each immunization. Red arrows indicate time points for immunization, and the yellow arrow indicates the time points when serum samples were taken. Importantly, the compound had a 100% responder rate, and from the second to the sixth immunization, as I mentioned, antibody responses were boosted after each dose.
Again, important, the placebo group, as expected, which is shown in green here, did not show any detectable signal, so that means any change in the signal. Now, the active immunotherapy elicits antibody in the periphery. The key question is now, do the antibodies reach their target in the target organ, in the brain? Therefore, we evaluated the titers in CSF as a proxy for the brain. Here, you can see that anti-PDA1 titers in CSF also increased with successive immunizations, demonstrating that the compound generates antibodies that can cross the blood-brain barrier. On average, IgG levels in CSF were an order of magnitude higher two weeks after the sixth immunization at week 76 compared to the third immunization at week 24. Here, we can conclude that antibodies which are induced in the periphery can cross the blood-brain barrier and can reach the target organ.
As a next step, we checked whether induced antibodies cross-react with the native alpha-synuclein sequence, and data are shown here, and you can also appreciate that we see again a strong increase in titers over time. Again, after each administration, a significant increase and overall a very high exposure and good reactivity, excellent reactivity against the full-length, against alpha-synuclein sequence, and in contrast, no change in the signal, as expected again in the placebo group. Now, we switch from pharmacokinetic parameters, so from titers to pharmacodynamic readouts, so to disease-relevant biomarkers. As I mentioned, the interim analysis demonstrates that anti-alpha-synuclein antibodies generated by the compound are engaging the target in the CSF, and what you can see here is the total alpha-synuclein content in CSF.
It is important to mention that as Parkinson's disease progresses over time, as I mentioned at the beginning, alpha-synuclein accumulates in the brain, and therefore, alpha-synuclein does not diffuse into the CSF to this extent as in the healthy state anymore. And as a result, you would expect to see a decline in the signal over time, and that's exactly what we have observed in the placebo group. You can see that the green line drops over time, clearly indicating less alpha-synuclein enters into the CSF. And in contrast, the blue line stays stable, stays flat, showing that we do not have any change in alpha-synuclein in CSF, indicating that antibody most probably reached the target in the target organ and prevents further aggregation.
Now, switching to another biomarker, we also analyzed neurofilament light chain, or NFL, which is a biomarker for neuronal damage, and here you can see results coming from CSF. Again, the NFL levels remained stable in the treatment group, again shown in blue, and increased in the placebo group, now in green again. Now, elevated levels of NFL have been reported as a sign of ongoing neuronal damage or neurodegeneration in various neurodegenerative diseases, and therefore, stabilization of neurofilament light levels suggests a slowing of neurodegeneration. In addition, treatment with 7104 might regulate levels of GFAP, which is a biomarker for astrocytic activation, neuroinflammation, and also for neuronal damage. Again, in blue, the active arm. In this active arm, GFAP levels remained stable until week 50, and at week 76, tended to decrease in this active group.
In the placebo group, plasma GFAP was elevated at week 76, as expected in Parkinson's disease subjects. Going to the next slide. Here, we share data on the dopamine transporter imaging. So dopamine transporter, or DaT imaging data, also suggests stabilization of Parkinson's disease pathology. DaT-SPECT is a nuclear imaging test that allows us to visualize dopamine transporters in the brain. And by measuring this striatal specific binding ratio, or SBR, we can quantify the density of dopamine transporter in this brain region. And lower SBR values indicate a synaptic function reduction in synaptic function. Now, in our interim analysis, DaT-SPECT scans show trends of slowing degeneration of midbrain dopaminergic neurons, as seen in the active arm, and as there was no progression in SBR values or change in SBR values up to week 48.
And this is in contrast, again, to the placebo arm, where we have observed a decrease in the signal, which is expected. Now, finally, we focus on the clinical measures. And here, you can see data on the MDS-UPDRS Part III, which is an examination of motor symptoms. And treatment with ACI-7104 limits progression of motor symptoms as measured by this score. This score is expected to increase by two to three or even four points per year in early PD subjects, and five-point increase in this is the threshold for a meaningful worsening of motor signs. And as you can appreciate, at week 74, the treatment group did not show signs or did show only signs of minimal changes, so signs of meaningful progression. And we see a stabilization in this score over the period of 74 weeks.
The placebo arm trended towards an increase in the mean total score. Maybe we skip this one here and go directly to the conclusion. Now, conclusion number one on safety and tolerability. I think it's really important to say that ACI-7104 has demonstrated a very favorable benefit-risk ratio to date. No clinically relevant or no serious adverse events were observed related to the study drug. And most common adverse events are transient and generally of mild severity, with expected injection site reactions, headaches, and fatigue. Conclusion number two, and here, I think this is really strong data we can share with you. We see a 100% responder rate that was observed after multiple immunizations. We see that antibody levels can cross into the CSF and therefore are present in the target organ.
We also clearly can show that anti-alpha-synuclein antibody levels were boostable and increased up to week 76. Finally, the data on biomarker and clinical measures. Now, we see a stabilization of total alpha-synuclein in CSF, which demonstrates target engagement in CNS, in the central nervous system. Total alpha-synuclein and neurofilament light chain in CSF suggested slowing of Parkinson's disease pathology, so disease modification. And plasma GFAP and DaT-SPECT imaging showed also trends for this stabilization. And in parallel to this, as I mentioned before, we see not just consistent trends in the biomarker, but this seems also to translate into a clinical measure, which means that ACI-7104 treated subjects showed trend to slowing of disease progression, as MDS-UPDRS Part III score was stable over time. And we did also this stratification by L-DOPA on/off state, and this again further enhanced the difference.
To conclude and to summarize now, I think we are really happy to share this data with you. I think we are very excited about the data showing that the compound is safe, that 7104 stabilized the disease-relevant biomarkers and clinical measures in this study, and this suggests potential for a meaningful clinical benefit to early-stage Parkinson's disease subjects, and, again, important, our goal is now to further develop the program and to discuss the clinical development plan towards registration with regulators, and with that, I will hand over to Andrea.
Yeah, thank you very much, Günter. That's wonderful. We are very excited by these early signs of efficacy, all pointing consistently towards the potential for ACI 7104 to slow Parkinson's progression. This data further underlines the potential and importance of active immunotherapies in delivering a precision prevention approach to neurodegenerative diseases.
In addition, our active immunotherapies in Alzheimer's, targeting tau and amyloid-beta, have already demonstrated in the clinic a number of clear advantages for the long-term use, including the long-lasting immune response, allowing an annual or biannual dosing regimen. We improved safety, and they come with an inherent economic and logistic advantage, which we believe may enable their realistic global application as preventive therapies. Our active immunotherapies and this new data on 7104 reinforce how AC Immune is pioneering precision prevention for neurodegenerative diseases. And I would like now to thank all the participants, the study participants, their families, all investigators, and the personnel for conducting the studies. And I would also like now to invite Professor Poewe to comment on the results, which we have just presented, in particular in review what these results could mean for patients, their families, and for treatment of Parkinson's in the future long term.
Werner.
Thank you very much, Andrea, for having invited me to be part of this meeting. First of all, I'd like to reiterate what Günther already pointed out. Parkinson's disease is the fastest-growing neurodegenerative disorder. It's growing faster than Alzheimer's disease, and the latest reports have shown a 273% increase in the global burden of disease for Parkinson's compared to 1990. So it's really an important disease. And while we do have very good symptomatic therapies for this disorder, we currently lack what is the most important unmet need, and that is slowing the progression of Parkinson's disease, something we call disease modification. This is the golden, the holy grail, so to speak, of all therapeutic endeavors and research into the treatment, all the more so since we're now able to recognize the disease even earlier than we used to before.
Now, targeting alpha-synuclein makes a lot of sense, and Günther has alluded to the central role that alpha-synuclein misfolding aggregation spreading has in causing disease and driving its progression. Now, what do these results we've just seen mean? First of all, they are impressive in the terms of immunogenicity of this vaccine, which is remarkably higher than previous vaccines were able to achieve. And we've seen, within the limits of an interim analysis of an early part of an ongoing study, within these limits, we're seeing exciting signals, at least from my point of view as a clinician who spent his life with Parkinson's disease patients, more or less, his professional life, that is. We've seen what was called stabilization of scores for motor disability, the UPDRS, which is the International Standard Scale to Assess Motor Dysfunction, mobility problems, tremor, all the facets of it in Parkinson's disease.
Now, what does that mean? Usually, one sees in early disease, and these were early patients, one sees these minimum of three-point increases on that scale over one year only. And here, we've seen results of more or less no change over 78 weeks in this interim analysis, still including a relatively small number of patients. But that's unusual. In itself, you might not be so impressed, but when you see it in the context of other measures, biomarker measures that are consistent, it gets really truly exciting for a clinical neurologist. We've seen one of the most important imaging parameters of progression of Parkinson's disease, of progression of neurodegeneration, the validated neurodegeneration marker we have in terms of imaging the brain is dopamine transporter SPECT imaging.
And that declines, and that's very well documented in many, many, many studies, that declines somewhere between 8% and 12% of that measure that Günther has introduced to you, the SBR. And here, we see no change in the treated, in the immunized patients. Admittedly, it's 25 people, but 25 people is not a small number for looking at this measure. So this is consistent with this clinical signal that we've seen. So what would this mean? If this is substantiated in the ongoing phase two trial and then translated into the clinic, it could mean two very important things. Number one, halting the progression of disability to the severe stages of Parkinson's disease that we still see, which end up in requirement for nursing home placements and terrible burden of disease.
It could open the door to early prevention programs, which are more and more a pressing need, as we learn, to recognize at-risk people for Parkinson's disease. So I, as you notice, I'm truly excited about these interim signals we've seen, and they can have tremendous impact if substantiated in this ongoing trial. I'd like to stop here and happy to take questions as they arise. Thank you.
Thank you, Werner.
I'll now ask the call operator to open the conference call to Q&A, and maybe we have some calls on the lines.
We will now begin the question and answer session. Anyone who wishes to ask a question may press star and one on their telephone. You will hear a tone to confirm that you've entered a queue. If you wish to remove yourself from the question queue, you may press star and two.
Questioners on the phone are requested to disable the loudspeaker mode and eventually turn off the volume from the webcast while asking a question. Webcast viewers may submit their questions in writing via the relative field. In the interest of time, please limit yourself to two questions. Anyone who has a question may press star and one at this time. The first question comes from Hama Shan from Jefferies. Please go ahead.
Hi, there. Two questions, if I may. So firstly, could you clarify why the CSF alpha-synuclein analysis was conducted post-hoc as opposed to a pre-specified analysis? And then secondly, in the phase one publication, there were reductions in oligomeric alpha-synuclein reported, whereas this release mentions more stabilization as opposed to the oligomeric forms. Was this measured? And if so, what were the results?
Thank you. Günther?
Yes. T o your first question, alpha-synuclein and all the biomarkers shown here were pre-specified in our statistical analysis plan. Therefore, they are part of the study. Now, the statistical analysis, and I did not point this out when I was at this slide. The difference between the active arm and the placebo arm was statistically or is statistically significant with a p-value of 0.018. This analysis was done post-hoc. But the analysis per se to go for total alpha-synuclein, this was predefined. That is the answer to your first question. The answer to your second question, we are now currently evaluating, or we are using a completely new technology to measure the composition of different alpha-synuclein species in CSF. So a technology which allows us to measure alpha-helical structure and to measure beta-sheath structure. This data will come now in the next weeks and months.
ADPD, yeah.
We aim to publish this data at the ADPD, yes.
Thank you very much.
The next question comes from Thomas Shrader from BTIG. Please go ahead.
Congratulations. This is a remarkably rich readout. So the neurofilament results are interesting. It's pretty noisy, and it's not a big signal in Parkinson's syndrome. I'm curious, do you have any correlation between patients that stabilized either there or with the dopamine receptor and who did well on the clinical scales? I know it's a lot to ask, but do you have a sense that the two results are correlated? And then on your biomarkers, have we seen everything? I'm curious if things like GFAP and some of the markers of synaptic health, are they good in Parkinson's disease, and did you measure them, and when would we see them? But again, congratulations.
I'd love to see another 500 patients, but it's a remarkable result. Thank you.
Maybe we don't need them, Tom. Günter, you do.
Yes. Thanks a lot for the congratulations. So for your first question, and we did not share this today, but we did the correlation between titer exposure in serum and in CSF and the correlation between titers and change in MDS UPDRS part three. And we have observed good correlation, inverse correlation, as expected, between the change in MDS part three and increase or titer fold increase, which is statistically significant. So that means in serum, we have observed a statistically significant correlation between titer exposure and the clinical scale on the MDS part three scale. We did the same for antibody levels in CSF. Again, the same trending, but here the p-value was a bit higher than 0.05.
Now, going to the second question, the GFAP, as you all know, these are measures which are not specific for Parkinson's disease, but still show, as GFAP and neurofilament light chain show changes or show progression in neurodegeneration. And we have to consider these measures as general measures for neurodegeneration. There are no particular measures for Parkinson's disease.
Great. Again, thank you.
Thanks, Tom.
The next question is from Ananda Ghosh from H.C. Wainwright. Please go ahead.
Hey, hi, Andrea, and team. Congrats on the data. I have two questions. The first one is on the DaT-SPECT data. One question is, as mentioned, there is around 5%-10% decline, which is seen in the natural history or as probably seen in other clinical trials.
My question is, when you say it's flat, is it absolutely flat, or is there some kind of 2% decline or 1% decline or something? That might be helpful to understand the importance of the data. And the other thing is, do you see signal in the putamen? And if so, what is the significance of that signal? That's my first question, and the second question will be on the dosing.
Yeah. Thank you for the question. I think, Werner, maybe it's a question for you.
Yeah. I think just to clarify, the striatal binding ratio on the dopamine transporter imaging is really sort of standard measure for neurodegeneration used, as you correctly indicated, used in a large number of trials.
I'm not aware of, of course, one can also subdivide the striatal into the putamen region and the caudate, but the striatal binding ratio in itself is the measure that is best validated where we know we have this between 8%-12% decline over one year, and then it progressively goes up in a kind of exponential fashion. In 25 patients, seeing what we see, as said, I think is an impressive signal. Numbers in the two arms are too small. The placebo arm is too small to speak about how much does it differ from placebo. But the active group in itself, to me, is remarkable.
Great. Thank you. My second question is on the very robust 100% responder rate.
Based on that, I mean, I was thinking, have you thought, have you kind of analyzed what's the half-life of these antibodies, which can actually inform us on how are you thinking about dosing the patients in the real-world setting?
Günther, do you want to?
Yeah. I think this is a very important question. The data we have up to now go to week 76. And at week 74, the last injection was done. Now, as I mentioned, we will follow up those subjects to week 100. And here, we can then clearly make a calculation of terminal half-life of the antibodies. But as we have observed at week 76, the strong increase in titers. And even at the time point when we went for the injection, titers went back to baseline.
I think we really have to consider whether injection every six months then in the real-life setting would make sense or on a yearly basis. But this final decision can just be done based on the data from week 76- week 100. But overall, we see extremely high titers and a good exposure over time.
Yeah. Maybe just one number, which Günther did not mention. We see at week 76 a 500-fold increased antibody titers over baseline. So that's something which has never been actually seen before with an active immunotherapy.
Got it. Thanks very much. And congrats again.
Thanks, Ananda.
As a reminder, if you wish to register for a question, please press star and one on your telephone. The next question is from Alyssa Larios from Leerink. Please go ahead.
Hi, everyone. This is Alyssa from Marc Goodman. Thanks for taking my question.
Congrats on the data. Somewhat similar of a question to one asked previously on the total alpha-synuclein levels in CSF. So just to confirm, that is its total measurements of alpha-synuclein, including all species of normal aggregated misfolded protein. Do you have an indication of how you guys are thinking about what you think is happening in the placebo group? Which species are being lost and which species are being stabilized in the treatment arm? Just to get your thoughts around that.
I think we have even a slide. Gary, you want to show the slide?
Answer to your first question, yes, it's correct. The data we showed are on total alpha-synuclein, which include all different forms of alpha-synuclein. Now, in this context, it's important to mention that in the CSF, most of the alpha-synuclein which is present there is the unfolded alpha-helical monomeric structure.
That means this signal is dominated by the monomeric alpha-synuclein, which is about 90%-95% of the total alpha-synuclein. But you're right, this signal also includes other alpha-synuclein species. Now, to the next question, as we go for the active immunotherapy, antibodies can cross the blood-brain barrier, and they are supposed to bind to the aggregated species of alpha-synuclein in the brain, resulting then in also microglial activation and reduction of those alpha-synuclein species in the brain. It's basically a clearance mechanism of alpha-synuclein in the brain, which also can result in higher mobilization of the monomeric form, but also the aggregated species into the CSF. We will see these results now soon. As I mentioned before, we go for this additional measurement, seeing the composition or testing, analyzing the composition of alpha-synuclein species in CSF.
And as Andrea mentioned, we are going to share this data at ADPD.
Thank you very much. Congrats.
Thank you.
The next question is a follow-up question from Sean Hammer from Jefferies. Please go ahead.
Hi, there. Two more questions from me, please. Firstly, in the press release, you mentioned a potential accelerated development pathway. Does that mean the current data supports skipping the part two and moving directly to a phase three trial? And then secondly, are there any plans to incorporate a tracer in the next study? Thank you so much.
Of course. Yeah, these are very good questions. So yes, we believe that we might actually change our development plan and accelerate the clinical development towards registration. So that's definitely something we will discuss over next week's or so with the regulatory agencies.
The second thing is, yes, we would love to include one of our tracer molecules potentially in a registration study.
Thank you so much.
So I think if there are no more questions on the lines, we have one question submitted via the platform. I'll go ahead and ask that one. That's from Paul at Noble Capital Markets. His first question is, do you think the next study in this program will have U.S. sites?
The answer is a clear yes, and obviously, we are looking for breakthrough therapy also going to the U.S., which is, I would say, very possible. Yeah.
And the second question is, can you move to the next study with your current financial resources, or would you have to conduct a raise?
I think, Chris, you want to answer that?
Yeah. Absolutely. Thank you. We are highly encouraged by today's results.
As Andrea mentioned before, we're currently evaluating the next steps, and we will ensure to allocate the required funding for further development of ACI-7104.056.
Thanks, Chris. I think that's it from our side. If there are no further questions on the lines or certainly on the platform, we would end the call there. I'll just wait for a moment to see if there are any other questions on the line.
We have a question from Ananda Ghosh from H.C. Wainwright. Please go ahead.
Hi, guys. Just one follow-up.
Given the interest in the field where you are seeing the passive immunotherapies going further and further to the preclinical or pre-symptomatic patients, seeing this data and as you are thinking about designing the next trials, and especially from your own experience from the TAU program, how are you thinking of including some of those preclinical or asymptomatic patients going forward?
Yeah. I think, Günther, you can follow me up to me. I think, again, a very good question, but I mean, we are very encouraged that we are actually seeing the stabilization of biomarkers clinical results in this early Parkinson population. So basically, disease modification. So I think the early Parkinson population will certainly be part of our next clinical trial. And I think it's also not quite advisable to generate the next clinical data in a population where you've seen so promising results.
Günther, maybe you want to add.
Yeah. No, that's exactly. So in the next clinical development phase, we will go for the almost identical patient population because, as Andrea mentioned, we have very nice data. And of course, now we have to substantiate this data, so we will not change to another population. But on the long term, I agree completely with you that it makes a lot of sense to go to a prodromal population. And this is also something we are currently working on, on developing a plan how to move at the later stage from early PD into a prodromal PD population.
Great. Thank you. So if there are no further questions, I think we'll close the call there. Thank everyone for the time they've spent today to join the call, and we're very excited by these results.
And hopefully, we'll have some more news to share in the new year with ADPD conference and so on. But in the larger scheme of things, this is all very positive for us. And so I wish you all a good day, and we'll speak again soon. Thank you.
Thank you.
Thank you.
Goodbye.
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