Q1 2023 Taysha Gene Therapies Inc Earnings Call
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Speaker 2: Thank you for standing by. This is the conference operator. Welcome to the TESHA gene therapies, first quarter, 2023 earnings conference call. As a reminder, all participants are in listen only mode and the conference is being recorded. After the presentation, there will be an opportunity to ask questions.
Speaker 2: To join the question queue, you may press star then one on your telephone keypad. To do need assistance during the conference call, you may signal an operator by pressing star and zero. I would now like to turn the conference over to Haley Collins, director, head of corporate communications.
Speaker 3: Please go ahead. Thank you. Good afternoon and welcome to TASHA's first quarter, 2023 financial results in corporate update conference call. Earlier today, TASHA issued a press release announcing financial results for the first quarter, 2023.
Speaker 3: A copy of this press release is available on the company's website and through our SEC filing. Joining me on today's call are Sean Nolan, Tasha's CEO , Supermarmadandran, President and Head of Research and Development, Cameron Alam, Chief Financial Officer, and Sam and Salmon Byte, Assistant Professor of Neurology at UT Southwestern.
Speaker 3: listing statements, including statements relating to the existing clinical data for TACHA 120, the therapeutic and commercial potential of TACHA 120 and TACHA 102. These statements may include expected timing and results of clinical trials for a product candidate, and other clinical and regulatory plans, and the market opportunity for those those who have
Speaker 3: This call may also contain four looking statements relating to tachyscroes, forecasted cash runway, and future operating results, discovery and development of product candidates, strategic alliances, and intellectual property, as well as matters that are not historical facts for information. Various risks may cause tachyscroes to differ materially from those.
Speaker 3: ability to obtain patent protection for our discoveries, limitations imposed by patents, owned or controlled by third parties.
Speaker 3: and the requirements of substantial funding to conduct our research and development activities. For a list in description of these risks and uncertainties that we base, please see the reports we applied with the Security and Exchange Commission, including our annual report on form 10k to the year and its December 31, 2022. The conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, May 11, 2023.
Speaker 3: Tash undertakes no obligation to revise or update any floor-of-the-team statements to reflect events or circumstances after the date of the top and call, except as maybe required by applicable security laws. With that, I would now like to turn the call over to our CEO , Sean Nolan.
Speaker 4: Thank you, Haley, and welcome everyone to our 20-23 first-quarter financial results and corporate update conference call.
Speaker 4: Today, I will begin with a brief corporate update. Then, Dr. Sukun Gandraan, President and Head of R&D of TASHA, will provide an update on our clinical development programs, along with our collaborator, Dr. Salman Bhai, Assistant Professor of Neurology at UT Southwestern. Camman Alam, our Chief Financial Officer, will then follow up with the financial...
Speaker 4: including the generation of first and human clinical data for TASHA 102 and adult patients with RUT syndrome. The submission of a CTA to the MHRA to initiate expansion of TASHA 102 and pediatric patients.
Speaker 4: The submission of an I&D application to the FDA, Vertesha 102, and obtaining further clarity from the FDA on the regulatory path forward, Vertesha 120 in GAN.
Speaker 4: Screening is completed and the dosing of our first potential patient with TASHA 102 and the Phase 1-2 Reveal trial and adult ret syndrome is scheduled for the second quarter of this year. For our GAN program, the new comprehensive analyses of the totality of the data for TASHA 120
Speaker 4: in a manner that clearly elucidates the potential for meaningful benefit to patients.
Speaker 4: We plan to submit the meeting request this quarter and expect the formal meeting to occur in the third quarter of this year. In the near term, we look forward to hosting an R&D day in June , where we will provide an overview of the GAN disease state and share these new clinical data analyses.
Speaker 5: As a reminder, TESHA 102 utilizes an innovative MIRNA responsive auto-regulatory element or MIRRAP platform to regulate the cellular expression of MECP2. At the upcoming ASGCT conference, we are excited to present new pre-clinical data that we believe supports the potential for TESHA 102 and the MIRRAP technology as part of a poster presentation on May 19. For our phase 1-2 reveal study in the RALP patients with red syndrome, we have completed screening and scheduled the dosing for the first potential patient.
Speaker 5: We expect the dosing to take place in the second quarter of 2023.
Speaker 5: We plan to report initial available clinical data which will be primarily on safety in the second quarter of the year at our upcoming R&D day. In the second half of the year, we plan to continue dosing adult patients with red syndrome in our reveal trial and provide quarterly updates on available clinical data thereafter.
Speaker 5: We plan to submit a CTA to the UK MHRA for TESHA 102 in mid-2023 to enable the initiation of a pediatric REP syndrome study. We also have an IND application submission to the USFDA plan in the second half of the year to further expand our clinical study footprint with TESHA 102. Now let's turn to TESHA 120 for the treatment of GAN, an ultra-rare neurodegenerative indication with no approved treatments or established regulatory pathway.
Speaker 5: As Sean mentioned, we are currently completing a comprehensive review of data from the ongoing natural history and interventional trial that includes functional biological and electrophysiological assessments.
Speaker 5: We plan to seek a formal meeting with the FDA to discuss a new analysis that FDA has not seen and regulatory paths forward for TESHA 120. As a reminder, early analysis based on MFM32, the primary efficacy scale discussed as the FDA type B end-of-phase-2 meeting.
Speaker 5: demonstrate a clinically meaningful slowing of disease, progression in patients with cancer, following treatment with TESHA 120 across the therapeutic dose cohorts.
Speaker 5: Importantly, long-term analysis points to sustained durability and the ability of TESHA 120 to prevent nerve degeneration, generate nerve fibers and preserve visual activity, which are significant findings for patients affected by neuro-degeneration.
Speaker 5: Importantly, over 6.0 years of long-term clinical safety data supports a well-tolerated safety profile with no major drug-related events. The FDA has stated that MFM32 can be a relevant primary endpoint in the setting of a randomized double-blind control trial.
Speaker 5: and acknowledge TASHA's challenge in executing and enrolling such a study design due to the ultra-rare nature of GAN. As such, the FDA indicated that it is open to regulatory flexibility in a control trial setting and is willing to consider alternative study designs, utilizing objective measurements.
Speaker 5: to demonstrate a relatively large treatment effect that is self-evident and clinically meaning. Our comprehensive analysis of the totality of data from the ongoing natural history and interventional trial which will inform our plans of future interactions with the FDA, continues to be encouraging and includes compelling new findings with potential.
Speaker 5: to further support a regulatory path forward. I will now turn the call over to our collaborator, Dr. Salman Bai, from UT Southwestern, who will provide a high-level overview of some of our initial analysis of the data for TESLA-120 in GAN and the clinical relevance to the disease state. Salman.
Speaker 6: Thank you, Suku, and hello everyone. My name is Dr. Selman Bay, and I'm an Assistant Professor of Neurology at UT Southwestern.
Speaker 6: I earned my medical degree and completed my neurology clinical training at Harvard Medical School with sub specialization in neuromuscular disorders. As a practicing neuromuscular neurologist, I'm keenly aware of the devastation that GAN causes, not only to patients, but also to their families.
Speaker 6: I've been working closely with Tacia on the development of the Tacia 120 program for over a year and a half and then energized by the opportunity to help bring a potentially transformational treatment to the GAN community.
Speaker 6: I've been heavily involved in the ongoing comprehensive analysis of the totality of data, and I've been working collaboratively with the team to identify new data findings.
Speaker 6: Based on the GAN clinical phenotype and pathophysiology, we are building a clinical narrative around the data to support our regulatory path forward for TASHA 120. I'm pleased to provide an update on the compelling findings from our ongoing data analysis.
Speaker 6: One goal of evaluating the totality of the data for TESHA 120 is to determine whether we can identify potential objective measurements that demonstrate a clinically meaningful treatment effect. For context, I think it's important to understand that GAN clinically manifests with marked in coordination a tax year.
Speaker 6: due to both severe central and peripheral nervous systems degeneration. We lead to significant disability and early mortality caused by respiratory failure.
Speaker 6: There is no approved treatment for this ultra-rare fatal disease. We have access to the largest natural history database of GAN to date through the NIH. As a result of our analysis of these data, we have a clearer understanding of how to measure meaningful treatment effect for these patients. For more information, visit www.nj.gov
Speaker 6: I'm a neurologist, so of course let's start with the neuroanatomy. We know there's central and peripheral nervous system degeneration with GAN. Specifically, this involves the cerebellum, long tracts, and sensory motor nerves.
Speaker 6: Clinically, these anatomical localizations translate to severe incoordination, which is ataxia, and weakness.
Speaker 6: We believe we have a comprehensive scale that we prospectively collected in the natural history and interventional patients, the Modified Frederick Ataxia Rating Scale, or MFARS, which was recently used as the primary outcome measure for drug approval for Frederick's ataxia. This scale is based on functional and objective measures within the neurologic exam focusing on ataxia, a key driver of disability in GAN patients. As a whole, we can prospectively measure the integration of the central and peripheral nervous systems using MFARS. We can then capture several objective peripheral nervous system data points.
Speaker 6: including nerve conduction studies, myometry, and nerve pathology.
Speaker 6: nerve conduction studies indicate sensory nerves recover responses that were absent prior to treatment, a key finding that was truly unexpected, and to my knowledge has never been demonstrated previously in GAN patients. We also see an increase in regenerative clusters on nerve biopsy. This is direct, electrophysiologic, and biological evidence of nerve regeneration. In a neurodegenerative disease, the peripheral nervous system data is key because recovery of sensory nerves directly impacts patients' performance on M-phars, providing links between objective, biologic data, and a clinical rating scale.
Speaker 6: Importantly, by developing a disease progression model through Bayesian analysis based on the natural history data, we showed that the progression of MFARS in GAN is predictable, monotonic, and homogenous across patients. Thus, we can use this model to determine treatment effect.
Speaker 6: Preliminary determinations of pre-manifact size relative to the disease progression model as measured by M-FARS and with multiple peripheral nervous system endpoints show disease slowing. Let me repeat, we have direct central nervous system and peripheral nervous system outcome measures and clinical and biological objective data.
Speaker 6: that show positive disease modification with TESHA 120. In an ultra rare, fatal, nerdy, generative disorder that has no approved treatment. The restoration of sensory nerve responses on nerve conduction studies and positive impact on other clinically relevant endpoints.
Speaker 6: show the potential for even greater clinical impact in this neurodegenerative disorder if treated at an earlier stage of disease with TASHA 120.
Speaker 6: I believe these data have the potential to provide objective measurements that demonstrate clinically meaningful treatment effects.
Speaker 6: We are truly, truly inspired by these patients and their caregivers. We are hopeful that we can bring a potentially transformational treatment to the GAN community. And we look forward to working collaboratively with the FDA through our anticipated future discussions.
Speaker 5: with that on our front-end call back to you, girl. Thank you, Salman. As you can see, we have compelling findings that we expect to submit as a part of our formal meeting request to the FDA in the second quarter of this year. These data will inform our discussions with the FDA regarding alternative study designs, additional objective measures, and ultimately a regulatory path forward.
Speaker 5: We anticipate a formal meeting to occur in the 3rd quarter of 2023. Importantly, administration of TESHA-120 also shows a translational correlation between pre-clinical and clinical studies.
Speaker 5: We saw similar clinical translational impact with spinal muscular atrophy and the SMN delta seven mouse model which we developed Zolgensma at AVEXIS, which showed improvement of stabilization in motor function and strength after treatment with gene therapy that for kangaroo has been seen in human studies as well. In June , we are excited to host a virtual R&D day where we will detail these new analyses and review therapeutic potential in the context of the GAN disease state as well as provide an update on our REDD syndrome program including new preclinical data for TESHA 102 in REDD syndrome being presented at the upcoming ASGCT annual meeting and available clinical data from phase one to reveal trial in adults.
Speaker 5: We continue to believe in the transformative potential of TESHA 120 and look forward to having a collaborative dialogue with the FDA regarding the potential registration path to bring TESHA 120 to patients with GAN who to reiterate have no approved treatments. I will now turn the call over to Cameron to discuss financials. Cameron? Thank you, Mr. Poo. Research and development expenses were $12.5 million for the three months that is March 31, 2020-3, compared to $38.2 million for the three months that is March 31, 2022. The $25.7 million decrease was due to reduced research and development compensation.
Speaker 7: as a result of lower headcount of $10.7 million. The decrease was also due to reduced manufacturing and other raw material purchases of $7.1 million. The decrease was due to reduced manufacturing and other raw material purchases of $10.7 million.
Speaker 7: We also incur $6.4 million reduced expense in non-clinical studies related to translational and toxicology studies, and $1.5 million lower expense in other research and development activities. General and administrative expenses were $8.8 million, but three months ended to March 31, December 20, 2023.
compared to $11.25 million but three months ended March 3rd, 2022.
The increase of $2.7 million was due to reduced general and administrative compensation as a result of lower headcount and reduced consulting and professional fees.
Net loss for the three months ended March 31, 2023 was $17.6 million, or $0.28 per share, as compared to a net loss of $50.3 million, or $1.32 per share, for the three months ended March 31, 2022. The net loss for the three months ended March 31, 2023 was partially offset.
will support planned operating, expected, and capital requirements into the first quarter of 2024. I will now turn the call back over to Sean for his closing remarks. Sean?
We believe that the clinical and preclinical data generated to date across our Rett syndrome and GAN programs reinforce our gene therapy approach and the therapeutic potential for our innovative programs to address severe unmet needs in monogenic central nervous system disease. In the year ahead, we are focused on executing across our near-term milestones in our Rett syndrome and GAN programs. In the second quarter of this year, we look forward to dosing the first potential adult patient with Rett syndrome and reporting initial clinical safety data for TASIA-102. We are excited to host an R&D day in June to review the analysis of the totality of the data for TASIA-102.
than two.
The first question comes from Yein Anju with Wells Fargo Securities. Please go ahead.
Hi, thanks for taking our question. This is Kwan An for Jana. And congrats on the progress. So first, the GAN program. So I wonder, thanks for the color on the new analysis. I wonder if the patient's data would be compared to their own control, like pretreatment progression.
or be compared to the natural history. And I wonder if there is a clear bar on what levels of change on those readouts, clinical meaningful. Thank you. Thank you.
Thank you for the question. I would ask Suku to take that first and feel free to add in.
Yes, so I will answer the question based on how I understood it and if I do not please, you know, clarify a question. So the analysis that is still ongoing, we do plan to compare each patient to their own pre-treatment status as well based on the natural history that has been collected by the NIH.
But we also have the option of looking at the broader data set in the natural history database where there were 52 patients with a mix of all types of GaN which include classic GaN and non-classic GaN. I would remind you that in these two types of GaN, the root cause of the disease is the same. Hence, the gene therapy and its findings, I think will lead to hopefully a very-
levels of change are clean, clean, meaningful.
It's important to understand clinically what's not only important for the patients, but also for the families. All right, a simple number on M-FARS that changes doesn't necessarily mean it's important to the patient. And that's why we work closely with patients and have interview with families, too, to identify what's most important from them. As a clinician, it's important for me to understand that patients are more likely to have M-FARS than those who have M-FARS. So we work closely with the families and help them understand that patients are more likely to have M-FARS than those who have M-FARS. And we also help patients understand
and we're looking at our data to correlate objective, biologic data with functional clinical outcome measures to define how that link is there and what it means for patients. When we have that data in totality, we are seeing positive trends, but of course this is preliminary.
We also use data from other diseases that have ataxia and peripheral nervous system disease to come up with correlates. You know, as you know, this is an ultra rare disease. So to clearly identify clinical meaningfulness for this disease alone is difficult and perhaps impossible. However, if we correlate it to other diseases and other clinical syndromes related to this, we can't.
we can come up with very good proxies that would give you a reasonable answer for what patients think is important.
Oh, got it. Thank you so much. The next question comes from Jack Allen with Beard. Please go ahead.
for gene therapies, I guess, namely, serpetas product in DMDs. And we realize that you're still discussing the regulatory pathways for GAN. But we're hoping you could provide some colors surrounding the correlations you're seeing between functional endpoints, such as the MFM32 score and the more objective biomarker endpoints, such as the retinol thickness, or retinol vein thickness, and neurobiopsy results. Thank you for listening.
Excellent question. When we take a look at functional clinical measures, of course there's an issue with sometimes there's bias or effort dependence and that's what we turn to biology. That's in the biology, that's where the question of accelerated approval can come in. So specifically if we're looking at sensory nerve action potentials, for example, something that we're seeing recover that was not previously there.
Well, that feeds into the feedback into your coordination for M-FARS and motor function as well. If you have de-affirmentation of your muscles, meaning you can't feel where your muscles are, your strength will decrease. And so having these kinds of markers correlate to clinical measures is important. We take it a step further because sensory nerve action potentials are electrophysiology.
the functional outcome measures and have a very clear trajectory of what's happening to the patient.
Does that answer your question? I'll see you guys later. Can I add a little bit of information which I think is relevant. As Dr. Salman walked you through to finish the second look at GAN, obviously it's an ultra rare disease. There's no therapeutic option available. Obviously you need an intervention where the benefit outweighs the risk.
looking at the model that we've generated, looking at the progression of the disease, looking at post-hoc analysis, what we're seeing collectively at this point in time is a trend when it comes to functional, physiological, biological, electrophysiological, and even potentially radiological impact of the intrathecal gene therapy that affects the broad spectrum of the disease in the central nervous system and the peripheral nervous system in a clinically meaningful way. So.
The next question comes from Kristin Kuska with Cantor Fitzgerald. Please go ahead. It's on wr Bible frequency.
Maybe you could add a little bit more color on the preclinical Rett syndrome data guided for ASGCT this month. How can we kind of put this into context as it relates to other data, other preclinical data we've seen from the program and what should we be expecting there? That's a great question. Let me stop, I think.
I'm very excited about the ASTCT data with the caveat that I can't speak about it in great detail because it's embargoed. So the date I think is in our press release but it's on the Friday, that's next Friday which is the 19th between 12 to two is when the information will be presented in front of the poster. So if someone is there hopefully you all will go review it. What is fascinating about gene therapy and you know I've been in drug development for a very long time.
But it's very rare, unusual, where I see preclinical data translate directly into the clinic in the human. I saw this with the SMA program when I was CMO, Chief Medical Officer of Access. I did comment that we are seeing this with GAN now, where the preclinical data appears to translate into the human based on the 14 patients we've dosed. And what I would say is that
The red preclinical data that's being presented at ASGCT next week is very interesting, but the details, as you decipher them, I think will hopefully show that we have a very good construct with the MRI technology that hopefully will be validated in this preclinical data set that will be presented next week. And to go beyond that, I'm also hoping that once we start dosing patients, both adults and hopefully children, that all this preclinical work that has been done in these different rodent models and other models.
Once again, if you have a question, please press star then one.
The next question comes from June Lee with Truist Securities. Please go ahead. Hi. Good afternoon. This is Mehdi for June . So given the ultra-rare situation for GAN, is it at all feasible to do a full-time job
double blind placebo controlled trial or not? And also for objective measures like M-FARS, is there the aim for getting a statistically significant change?
for these indications, for these measure. And if that again, given the ultra rare situation, is that possible or not? Thank you. Excellent question. When we think about ultra rare diseases like this, first we come into a question of what's the practicality of doing an RCT?
But with this disease, when we have natural history as a control, it serves as a powerful comparator arm. Now that we have several other patients within the natural history to compare to the intervention, we can determine treatment effect and find statistical significance.
MFARS, as you mentioned, is objective. It's, of course, the neurologic exam, which I love. So that adds some objectivity to it, and we're able to detect changes, especially when we use the disease progression model, to show differences. The next step is to find clinical meaningfulness in that data, and that's our hope with the biology, the histology, the electrophysiology to the...
The conventional data that we have is also the largest for a disease like GAN. The third thing that the NIH and we've discovered in the natural history study is that all these patients have ataxia and therefore makes them far as an appropriate clinical measure to see the efficacy of the product. Right, do you agree, Norman? Yeah, the neuroanatomy fits perfectly what we're seeing in patients and 100% have ataxia. So why not measure that and why not measure the efficacy?
because they thought it was effort-based. And when we asked them for clarification around that, they did come back and acknowledge that in this type of a disease state with an ultra-orphan population, you could not feasibly conduct that study. But they also then went on to say, and reinforce published guidance.
that a well-controlled trial that has clinically meaningful endpoints that are objective would be considered. And hopefully what you're getting a flavor for here and that Dr. Bai is providing additional color on is that, you know, as we've interrogated the database, and as Suku said, it's the largest database in the world for GAN.
we're seeing across multiple clinical domains that affect both the CNS and the PNS what we think is clinically meaningful impact on objective endpoints that are unequivocally objective.
And so that's why we're so confident, or I should say encouraged, by the data that we're generating thus far. And we look forward to, you know, showing it in much more detail at the upcoming R&D day. Can I add a point to that too? With the natural history data, what's crucial for this model, which we've shown...
is that it's homogeneous, it's predictable. And based off those reasons, we can now use that model to compare to our intervention patients. Awesome. So, if I may, like, I reformulate the question and ask it a different way. If M-Force was the primary objective from the beginning, would that...
trial data so far make it convincing for FDA to approve the drug? Awesome question. In hindsight, when we take a look at this data, it's clear. We look at the neuroanatomy.
It's quite clear, but with an ultra rare disease like this, it's always a struggle. What's the initial hypothesis and what are we getting? So if we were to go back and make that the primary, of course, right? This is a disease that has a taxi and 100% of patients, and those are the findings that we're seeing that we believe to be clinically meaningful. And I would add one more thing to what Dr. Bhai just said.
into a clinically meaningful effect that could be far greater if the children were treated much earlier given that the neurodegeneration may have not progressed as much. Obviously, as the Thaviyati by saying, we haven't studied children younger than six years away and we have great interest to see, you know, if you can have that kind of significant significance as well, impact in younger patients as well. So, collectively we are very encouraged with the data that we have seen and looking forward to meeting with the FC and talking.
Good night everyone. Good night everyone. This is Gil on for Gil.
Maybe a good place to start is just to help me understand the order of events.
So you're having your R&D event, the head of an FDA meeting in the third quarter. Why not the other way around?
So that's a good question. So keep in mind though that we are putting the meeting request in in the second quarter and there is going to be a certain time lag before we actually get the meeting hopefully. But at the same time, we are generating significant amounts of data from pre-specified endpoints post-token.
And the ethical platform, what kind of impact would it have across a broad aspect of neurodegenerative and neurodevelopmental disorders? And I would again remind you that if you look at the SMA program with Jolgensva, the IV formulation has significant impact in SMA type 1 and some other sub types as well. But recently, Novartis released more data with the Intersecal approach where there was significant physical impact in SMA type 2 type 3.
the other thing to add to that is that in a perfect world, there would be a scientific conference that lines up with us, and that would have been the preferable way to disclose things. But in all candor, we step through this analysis not knowing exactly what the outcomes are going to be.
And at this point, we're very encouraged by what we're seeing. And you hopefully can tell from the way we're coming across on the call that, that we feel this is very compelling. And so we thought that was the best way to disclose it, explain how we were going to move things forward with the agency, and highlight our rationale and then provide the data, that an RV justifies our conviction with the program. Okay, that's fair. And bear with me here for a second, because this is a little complicated. So syrup, uh, is.
So as a neurologist, of course, I would say that it is. So for example, if you hold your arms out in front of you, if you happen to have a headset on, and you take your right pointer finger and touch your nose, there's a little bit of jitter there. Now to most people that might not be much, but to me, I can pick that up. Now if you have even more jitter, I can pick that up further and start to objectify what your exam findings look like. And so that's M-FARS. M-FARS.
So not only are there objective pieces from the neurologic exam there that I can point towards and say, this has intra and interrater reliability, but there's also objective measures that then back that up. So if I was a bad neurologist and not diagnosing correctly, I have objective measures there to help support that. But MPRS, I would argue, has objective measures within that.
Okay, because in my opinion, I think that might go to the heart of the matter because it's really obvious that the FDA doesn't like external controls when it comes to things that can be trained in open label study.
And also like the Riyadhah product that was approved with M4. So you know there is a, exactly but there is a history on the regulatory side you know that sometimes it's just in practical to ask for under my specific control trials and perfection, it comes with technical trials design but when there is no therapeutic option available.
and these kind of studies, especially in ulterior disease, show clinical benefit, I think that it becomes a negotiation between the regulatory agencies and the sponsor in making sure the product is appropriately made available to the patient community in question. And I would go even further to state that Peter Marks and colleagues have been out there obviously encouraging a serious discussion between the agency CBER and the sponsor of this kind of ulterior disease program.
in having some flexibility if the benefit for elsewhere is the risk. And there's no other therapeutic option available to the patient community such as in GAN, which is frankly a terrible disease. If you meet these patients and families and see what happens to them, I think that that way is now open for us to appropriately position our data, talk to the FDA and show them that we ourselves are convinced and hopefully we can convince them that it's an appropriate product.
and MRIs, right? So to show that no matter where you're kind of cutting the bread, you're getting an effect in all these domains that can only be attributable to the drug.
And, you know, I think with the model that we've got put together, we have a very scientifically driven data driven.
control that we can point to and this highlights the effectiveness across all these different domains. So, put very simply, we're not hanging our hat on any one thing. It is the totality of the data. Okay. Thank you for taking out our questions again. I'm going to come back to on the progress. Thank you. Once again.
rest of your day. Take care.
This concludes today's conference call. You may disconnect your lines. Thank you for participating and have a pleasant day.
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