Greetings. Welcome to CervoMed results from week 32 of phase IIb RewinD-LB study. At this time, all participants will be in listen-only mode. The question and answer session will follow the formal presentation. If anyone today should require operator assistance during the conference, please press star zero from your telephone keypad. Please note this conference is being recorded. At this time, I'll hand the conference over to Bill Elder, Chief Financial Officer and General Counsel for CervoMed.
Bill, you may begin.
Welcome to the CervoMed conference call. This is Bill Elder, Chief Financial Officer and General Counsel for CervoMed. Today we announce 32-week data from the extension phase of phase IIb RewinD-LB trial in patients with dementia with Lewy bodies, which were presented over the weekend at the AAIC conference in Toronto. Even considering the previous 16-week extension phase results, which demonstrated a clear clinical effect of neflamapimod based on the primary endpoint as well as other measures, the week 32 results from the extension phase add meaningful further evidence of neflamapimod's potential ability to slow the progression of this devastating disease. The durability of effect that we are observing further increases our confidence in the probability of success in a phase III trial. Today on the call, Dr.
John Alam, CervoMed CEO and co-lead investigator of the RewinD-LB study, will discuss the DLB opportunity, the new data, and our path anticipated forward. Before we begin, I refer you to our Safe Harbor statement on slide 2 of today's presentation. We will be making forward-looking statements on this call, and actual events and outcomes could differ materially. Please consult our SEC filings for a complete discussion of risk factors related to others. I will now turn the call over to John Alam. John?
Thanks, Bill. To frame today's discussion, CervoMed is developing new treatments for the treatment of neurologic disorders. In particular, we are focused on a major clinical and commercial opportunity, the treatment of dementia with Lewy bodies with our lead asset, neflamapimod. We demonstrated proof of concept with neflamapimod in phase IIb trial results that we reported earlier in 2025. The 32-week extension phase data reported at AAIC announced today further confirmed the potential of neflamapimod to slow the progression of disease, and I will go through the key new data in detail. I will close by discussing the anticipated next steps for the program, and then we will invite analysts and investors into Q&A session. I'll start with the opportunity for neflamapimod in DLB. Dementia with Lewy bodies is a progressive brain disorder that affects thinking, movement, and sleep.
The average time from diagnosis to requiring a nursing home is only two years. DLB is distinct from Alzheimer's disease, which progresses more slowly and has a very different pathology. DLB is characterized by abnormal clumps of protein of a protein called alpha-synuclein in the brain and otherwise called Lewy bodies. Clinically, there is a progressive decline in cognitive abilities and movement problems associated with movement problems similar to Parkinson's disease. Visual hallucinations are also very common. There are currently no approved treatments for DLB in the U.S. or EU. It is an untapped opportunity with a large and accessible patient population. In the past 10 years, there's been a wave of research advances and insights that have shed light on the molecular mechanisms of DLB, and this is a paving way for the potential development of the first truly effective treatments that address the underlying cause of disease.
There's an important aspect to DLB about the progression of disease and rapidity of decline, which makes it more severe and a more devastating dementia compared to Alzheimer's. It also makes it possible to see disease-modifying effects of therapy with relatively short clinical trials using well-characterized endpoints. We are targeting the subset of patients who are diagnosed with what we would call pure DLB, that is DLB with no evidence of Alzheimer's disease co-pathology. This is a highly valuable opportunity with an initial target population of 175,000 diagnosed patients who have high unmet medical needs. Acetylcholinesterase inhibitors, such as Exelon or Aricept, are commonly prescribed in DLB, and they are known to provide transient improvements in cognition, but no improvement on motor function. There are currently no approved therapies that address the drivers of disease progression in DLB.
What drives the clinical symptoms and progression of DLB has become much more clear over the past 10 years, and this sets the stage for the development of truly targeted therapies that can potentially change the course of this rapidly progressive disease. Specifically, in DLB, in the basal forebrain cholinergic system, the buildup of alpha-synuclein and neuroinflammation leads to hyperactivation of the alpha isoform of p38 MAP kinase, which is a primary target of our drug neflamapimod. P38 hyperactivation, in turn, leads to increased tau phosphorylation, impaired retrograde axonal transport, impaired NGF signaling, and reduced acetylcholinesterase release, and ultimately synaptic dysfunction in cholinergic neurons, which is now well established as a major driver of disease expression in DLB. From a clinical trial perspective, a key enabling innovation for evaluating DLB patients is the ability to identify and exclude patients who have Alzheimer's disease co-pathology.
It has been demonstrated convincingly that elevated levels of phosphorylated tau in the blood marker in the blood are a marker of Alzheimer's disease pathology in the brain. A simple blood test now can be used to identify tau and amyloid pathology and obviate the need for PET scans. We have used the cutoff levels of plasma tau in our clinical trials to identify patients who don't have AD co-pathology, and it has given us important insights for understanding clinical improvements in DLB as well as planning for a potential phase III trial. I will touch upon both points later in my remarks. Turning now to phase IIb trial results we reported earlier this year.
RewinD-LB is phase IIb clinical trial of neflamapimod that enrolled 159 patients with a diagnosis of dementia with Lewy bodies, and who were verified to have low baseline levels of plasma pTau-181 in screening to ensure that we had enriched for patients with pure DLB, that is DLB patients who do not have AD co-pathology. The first 16 weeks of the trial were placebo control, and we learned that the neflamapimod capsules used in the initial dosing period yielded suboptimal plasma drug levels. When patients subsequently received new capsules that delivered target exposures in the extension phase of the study, we saw clinical improvements on the primary endpoint as well as other secondary endpoints, establishing proof of concept for neflamapimod as a treatment for DLB.
The primary endpoint for the RewinD-LB trial is the CDR Sum of Boxes, which is an established gold standard endpoint for evaluating severity of disease and clinical progression in dementia of all different types. A 0.5 point increase in CDR Sum of Boxes, or CDR-SB, represents a clinically meaningful worsening of the dementia. In untreated DLB patients, the median increase in CDR-SB is approximately 1 point over 24 weeks, indicating the rapidity of clinical decline typically seen in patients with DLB. Here are two key parts of the results we reported back in March at the 16-week time point of the extension phase. The graph on the left shows a primary endpoint in patients with screening plasma pTau levels less than 2.2 pg/mL. In this subset, we saw a 67% relative reduction in CDR-SB with the neflamapimod new capsules.
The graph on the right looks at patients who had significant worsening of disease, a greater than 1.5 point increase in CDR-SB by the end of the 16-week extension phase. Here, what we see is a 62% relative reduction of patients with clinically meaningful progression in patients who received the new capsules as compared to what was seen in the control group or the patients who received old capsules. I'd like to now walk you through the results we announced over the weekend, the 32-week results from the extension phase. As Bill mentioned, the 32-week results add meaningfully to our understanding of neflamapimod's potential clinical effects, and they further increase our confidence as we prepare to meet with regulatory authorities and align on our potential phase III design for neflamapimod.
This slide shows how the new capsules were introduced into the extension, with the majority of patients receiving old capsules at the beginning of the extension phase, while nearly all patients after the week 16 time point in extension were receiving the new capsules. As a result, the duration of treatment with either old or new capsules is variable. That is not, for example, that they received a fixed 16 weeks or 32 weeks of treatment across the board. As a result, the most robust and appropriate analysis is a Kaplan-Meier analysis with a dichotomous outcome, such as clinical progression or not. For most of you, this type of analysis will be very familiar because, for the very same reason, variable lengths of follow-up, this is a routine analysis used in cancer trials.
The key data that we presented over the weekend was this Kaplan-Meier analysis timed to meaningful progression of all patients in the study through the 32 weeks of treatment. Both the Kaplan-Meier analysis and the definition of clinical progression, a 1.5 point increase, were pre-specified in an addendum to the statistical analysis plan that was implemented in early February. The analysis looks at progression-free survival for all patients who entered the study, i.e., it is an intention-to-treat analysis, and it is a robust measurement of the proportion of patients who experience significant clinical worsening that takes into account the variable lengths of treatment that patients receive with old and new capsules.
Although the CDR-SB is inherently designed so that a true 0.5 point change is clinically meaningful, the higher cutoff of 1.5 was used in this analysis to mitigate against the impact of individual variants in order to allow for a more robust evaluation of the treatment effects. In the slide, we have shown the placebo curve in addition to the old capsule and new capsule curves. You can see very readily in the first 16 weeks, placebo and old capsules are very similar in terms of rate of progression, with a high rate of progression out to the first 16 weeks. With old capsule treatment, the progression continues on the same trajectory.
In contrast, among patients who are getting new capsules, there's a dramatic slowing of the number that experience clinically significant worsening, and the gap between new and old capsules gets even wider between week 16 and week 32 of the extension. You can see the p-values for the comparison between new and old capsules, which is highly significant.
In addition, when we look at the hazard ratios, which is the risk of progression in new capsules compared to old capsules, what we see is that with new capsule treatment, there is a 54% reduction, a hazard ratio of 0.46 with the new capsule treatment relative to old capsules, while in the patients with the more stringent criteria for AD co-pathology, a screening plasma pTau level less than 2.2, the hazard ratio is 0.36, reflecting a 64% reduction in the risk of progression with new capsule treatment compared to the control of old capsule treatment. Using the same Kaplan-Meier analysis and comparing different cutoff levels of plasma pTau-181 at screening, it was shown that using a cutoff lower than the 2.2 pg/mL level does not further reduce the risk of progression. We believe this is important new information as we prepare for a potential phase III trial.
Next, I'd like to highlight very recently obtained plasma glial fibrillary acidic protein, or GFAP, data that we released today in association with the AAIC presentations in our press release, which data that we believe provides further validation of the impact that neflamapimod has on the underlying disease process. As many of you know, GFAP is a well-established blood-based biomarker that reflects injury or stress in astrocytes, key supporting cells in the brain. More importantly, in the context of neurodegenerative disease, perhaps reflecting the astrocytic response to neuronal damage, scientific publications and data have shown elevated GFAP levels in the blood are associated with active neurodegeneration in the major dementia, and the plasma biomarker that is one of the most consistently linked to cognitive decline and disease progression in various diseases, including and particularly in DLB.
Moreover, in the patients who do not have AD co-pathology, GFAP is the first biomarker that is elevated in the course of the disease and ahead of neurofilament light chain. These new results show a meaningful and statistically significant reduction in plasma GFAP levels in patients who were on new capsules in reduction from the start of the extension phase through to week 32. Specifically, over the 32-week extension phase, GFAP levels declined by approximately 18%. By contrast, during 16 weeks of placebo administration, which reflects the course of GFAP levels over time without treatment, the levels increased about 1%. Similar to the other data we've shared, patients with a baseline plasma pTau less than 2.2 pg/mL saw an even greater treatment effect, in this case with respect to greater decline in plasma GFAP levels.
The GFAP data, combined with the 32-week clinical data, we believe provide unambiguous demonstration of proof of concept for neflamapimod as a treatment for DLB, specifically in the patients with DLB who do not have AD co-pathology. Our key takeaways for neflamapimod from the AAIC data presentation of today's data release can be summarized as follows. The slowing of clinical progression that was identified at the 16-week extension phase time point has been sustained out to 32 weeks of treatment. The benefit seen with neflamapimod is clinically significant. Patients who received neflamapimod for up to 32 weeks in the extension phase showed a 54% reduction in clinically significant worsening on the CDR Sum of Boxes compared to patients who received control. This reduction improved to 64% among patients who had minimal evidence of AD co-pathology.
The effect on clinical progression was associated with a significant reduction in plasma levels of the neurodegenerative marker GFAP. Results that further corroborate that neflamapimod has achieved proof of concept as a disease-modifying treatment for DLB. Finally, we believe that for plasma pTau-181, the cutoff level of 2.2 pg/mL is optimal to define the presence or absence of AD co-pathology in the context of neflamapimod treatment. With that cutoff, patients with what would then be called pure DLB represent about half the DLB patient population. Turning to our anticipated next steps for the neflamapimod program. With the data we have gained from phase IIb trial, we are now poised to move into phase III. We first gained proof of concept data earlier this year. We have now further strengthened our understanding of how neflamapimod's treatment effect on slowing of clinical progression is sustained.
We are now planning to meet with the FDA in the fourth quarter of 2025 to reach alignment on a phase III trial design. The RewinD-LB trial and the extension phase were very data-rich, and we believe give us all the clinical information we need for a potential phase III trial, including duration of therapy, effect size, number of patients, and the use of plasma Tau levels to identify patients. We can now project with that much more confidence a phase III clinical trial of neflamapimod that looks very similar phase IIb and can demonstrate efficacy that may support approval. We expect the pivotal clinical trial design will look very similar to phase IIb RewinD-LB trial. We plan to enroll DLB patients who don't have AD co-pathology, as determined by blood tests for levels of phosphorylated Tau. We expect to use CDR-SB as a primary endpoint.
We expect to enroll at approximately 40 sites. While RewinD-LB was 16 weeks in initial duration, we currently expect, and consistent with ICH guidelines, a phase III trial will be 24 weeks in duration and subject to further discussion and alignment with the FDA anticipated in the fourth quarter of 2025. The fact that we have sustained clinical benefit phase IIb at 32 weeks of the extension phase and also a widening gap between treated patients and those patients who received control gives us confidence as we head into this potential phase III trial design. To recap the main points around neflamapimod, DLB is a distinct dementia where progression is rapid. This creates an opportunity to see significant clinical effects in short-term studies.
We have seen encouraging effects phase IIb, first with the 16-week extension phase data, and now a more pronounced effect at 32 weeks of treatment. This gives us confidence that we may achieve positive phase III outcome, with a phase III that will be very similar to phase II in terms of design, subject to further discussion and alignment with the FDA. There is a high unmet need in DLB, and we have fast-tracked designation for neflamapimod in this proposed indication. We know that investigators are looking forward to getting a phase III trial underway, and we are focused on bringing neflamapimod to the market as quickly as possible. In closing, we believe we are well positioned with a de-risk late-stage asset and a potential rapid path to market in an area where there are currently no approved therapies.
DLB is a high-value specialty disease, and that the first disease-modifying therapy of DLB has multibillion-dollar potential. We believe that first therapy can be neflamapimod. We have multiple significant milestones in the near term, including the planned trial of the start of a phase III trial. CervoMed is led by a strong management team, board, and advisors, and we are committed to the pursuit of this opportunity. Thank you. I will now open the call up to questions.
Thank you. At this time, we'll be conducting a question and answer session. If you'd like to ask a question, please press star one from your telephone keypad, and a confirmation tone will indicate your line is in the question queue. You may press star two if you'd like to withdraw your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment, please, while we poll for questions. Thank you. Our first question comes from the line of Sumant Kulkarni with Canaccord Genuity. Please proceed with your questions.
Good morning. Thanks for taking our questions, and it's very nice to see these 32-week open-label data backing up what you saw at 16 weeks. How would you translate these data to what you might need or expect to see in a phase III in terms of a clinically relevant change in the CDR Sum of Boxes, and what specific dose do you expect the phase III to involve? I have a follow-up.
On the first question, I think what we've shown in terms of either the correlation, in particular, what we've shown in the 32-week data with the time to progression defined as a 1.5 increase in CDR Sum of Boxes, that is inherently a clinically meaningful result. That level of impact on the CDR Sum of Boxes inherently is clinically meaningful, and that's the fundamental argument that we're making that the results in the 32-week results in particular would translate into a clinically meaningful effect in a 24-week phase III trial. I think what we've seen, both in terms of mean change and in terms of time to progression of a 1.5 point increase, which could also be in a full phase III trial, could also be translated into just the number of patients who progressed within a six-month time frame. Put together in that way, again, is inherently clinically meaningful.
That's why we think that the effect that we're seeing really informs very strongly in terms of a 24-week phase III trial being able to demonstrate the benefit-risk ratio that you need to be able to demonstrate for approval. In terms of dose, I think the combination of the biomarker data, as well as the 32-week data with the sustained effect out to that point and the magnitude of the effect in terms of in the intended targeted now patient population with a 64% reduction in risk of progression, that's a clear-cut demonstration of the 40 mg TID dose level, the blood concentrations in particular that we're achieving, drives a clinical effect that would be meaningful and would have a real impact on the lives of patients with DLB. That really is, in the end, ending up as our target.
It's the 40 mg TID dose and being able to achieve that average 5 ng per mill C trough level.
Got it. Thanks for that. On GFAP, we know CDR Sum of Boxes is going to be the primary endpoint in your phase III, but how receptive do you think the FDA might be to utilize GFAP as a regulatory relevant metric, and is there any consensus on what might be considered clinically relevant reductions?
I think that at this point, I'll just say that I don't, again, that it is fundamentally, it supports the clinical results in terms of specifically with respect to an effect on clinical progression. I think the FDA, I think, would think along the same lines. It is that fundamentally, and that the drug is acting on the underlying disease process. I don't know if you were trying to say that would they take that as a measure or could that be a surrogate endpoint. I don't think at this point it's at a point where it's a surrogate endpoint where you could get approval based on that alone. An objective marker such as GFAP and a neurodegenerative disease marker is inherently in these contexts, you know very well, just strengthens the fundamental argument that you are impacting clinical progression.
There's no set cutoff, but I think it is just that this is, there are very few drugs that have shown an impact on GFAP and certainly none in DLB. The effect we're seeing, it's very clear-cut. There is a reduction in GFAP levels. Remember that this is, in the end, confirming what we presented in phase IIa, where the GFAP reductions we were seeing were actually correlated to the CDR Sum of Boxes result. Across the board, in a variety of different settings, longitudinal increases in GFAP of relatively modest amounts are strongly correlated to cognitive decline as well as disease progression overall. I think it just, it's a, this is a great result to be able to see that, particularly in the context of the 32-week result.
If you put the two together, just very clear-cut evidence that we are impacting the underlying disease process and with that, substantively slowing clinical progression.
Thank you.
The next question is from the line of Soumit Roy with Jones . Please proceed with your question.
Good morning, everyone, and congratulations on the improving data. One point, I don't know if I missed it, have you presented the CDR-SB score at 32 weeks? The second part is, how does the compliance look like in these patients in terms of the medication?
On the first point, yes, we have not, it's not in the press release, but we did look at the mean change in patients who receive 32 weeks of old capsules and 32 weeks of new capsules. The relative effect is qualitatively very similar. There's about a 40% reduction in all participants and a 50% reduction in the patients whose screening pTau-181 level is below 2.2 pg/mL. The reason we didn't put that in as the main analysis in the SAP and NORA reporting as our primary analysis of this data is that inherently, it's a completer's analysis, and it's biased in many respects. With the old capsules, you have more patients progressing, and they're dropping out. The patients who remain behind are inherently going to be the less likely to progress patients.
It is a result that, as it's a little bit less than the Kaplan-Meier analysis, which is a true intention-to-treat analysis, is not actually that surprising. Soumit, you've heard me say this about many other trials that are published. I think a completer's analysis inherently, when you have an imbalance in terms of people dropping out, it's a hard part to go to. We've done the sensitivity analysis, and it more or less looks the same. We're not reporting it here because we define as the analysis we're going to do at 32 weeks of treatment is the time to progression analysis. A priority, we define it that way. In terms of adherence, the monitoring that we've done, it's actually very good. Certainly, people are not missing doses.
What we hear is that they're following, if they do miss a dose, they do exactly what we advise, which is at your next dose, you just double up on the dose. What they come back with is across the board, they've taken all their pills during the time period that they're assigned.
That's very reassuring. Just trying to understand your thinking around the FDA conversation, are you going to wait for the French trial to read out and bring in that data along with this updated data from the extension arm? If the French trial with the TID dosing really shows much more improved, how would you present it to the FDA for dosing, or would you stick to the phase II U.S. trial dosing?
At this stage, the intent in our communication today is that with the data that we've seen now at the 40 mg TID dose level, both the clinical progression data and the magnitude effect there, along with the plasma GFAP effect, we're going forward with the 40 mg TID dose level. That's why we're communicating now that our intent is both with FDA and with EMA. We are planning on, or we expect to meet with them within the fourth quarter. We're not waiting on the Strasbourg data at this point. We're really very much the BID regimen, higher dose regimen. We consider that at this stage, you can think of it more along the lines we had talked about last fall, Soumit. You know this, that's more a little bit of lifecycle management, give us more flexibility and give patients and physicians more flexibility down the line.
The data, what we're seeing here, says that in a context like DLB, where there's a high medical need, what we're seeing justifies going forward with the 40 mg TID dose regimen.
Thank you. One last question, trying to assess the urgency or how proactive you are in business deals in the ex-U.S. territories, is that something you're actively pursuing for partnering or licensing out China, Japan, or EU territories?
I'm not going to give you any specific timeline or what discussions we're having, but we have said, and we continue to believe that a regional licensing deal, either in Europe or in Japan or maybe even farther East Asia, is something we're very much open to. I think there's multiple different reasons why the specificities and the opportunities in those areas are such that there are likely to be companies who would be interested in that discussion, and that's something that doesn't change in all of this, as in from a business standpoint, if nothing else, in Japan in particular, to maximize our opportunity there, but also to provide opportunities to get financing for the core program in a non-dilutive manner.
We're absolutely open to it, but I can't, I'm not going to give you, I'm not in a position to actually give you more detail than that as to whether we are in active discussions or not.
Certainly. Thank you again for taking all the questions, and congrats on the data.
Thank you very much.
Our next question is from the line of Raghuram Selvaraju with H.C. Wainwright. Please proceed with your question.
Thanks very much for taking my questions, and congratulations once again on all the progress. I was wondering if you could just summarize for us the scientific evidence correlating the reduction in GFAP levels in plasma to the impact on astrocytic activation and neuronal health in the brain. You know what's historically been published around that and the extent to which you can correlate the plasma reduction to the actual impact in the context of the CNS. Secondly, I was wondering if you could just recap for us how you expect discussions with the FDA to proceed from here and what we can expect as sort of the next milestones, gating items on the regulatory front as you look to firm up the regulatory path underlying clinical development activities for neflamapimod.
I'm not going to go through, I can't, I just, you know I can't give you the specific citations up front, but if you go to my CTAD presentation last year on GFAP, which is on our website, there's a set of citations that are in one of the slides. GFAP levels have been correlated even in pathology to both neuronal loss and in particular to tau pathology. This is probably the most, in an all-comers dementia evaluation, which is the most direct, and that's one of the strengths of GFAP. It actually was not correlated to amyloid plaque levels. It's specifically to the neurodegenerative process, and in particular to neurodegenerative processes that are Tau-driven, as in DLB and in our mechanism downstream of inflammation is tau and pPA activation is tau hyperphosphorylation.
That was published last year and really put, I think, in many respects, puts an exclamation mark into all the other clinical correlations between cognitive level and GFAP levels in both Alzheimer's disease and in DLB. That's a correlation that was in our phase IIa data. You could correlate the CDR Sum of Boxes score at baseline to GFAP levels. We actually internally validated it in our phase IIa result. Now, what level of reduction with treatment leads to what level of clinical effect? I think that's an imponderable without actually having drugs. That would not be inherently. It's not going to be there without having drugs that actually do that, enough data to actually go to what is the level of GFAP progression decline.
If there's one example, and it's going to be all mechanism-related, both lecanemab and donanemab, the one biomarker where there's a clear-cut effect on is the GFAP levels. That biology is completely consistent in that oligomeric A-beta is going to activate, is known to activate microglia and astrocytes. If you block that, you're going to have an effect in terms of the astrocyte activation and GFAP levels. In our context, I think it's more the same argument, and again, it's in my presentation before, that GFAP levels, when you really look at the pure DLB population, is reflecting the cholinergic degeneration and dysfunction in the basal forebrain. This is just clear-cut evidence that we're impacting that process. In general, biomarkers like this, which end up being a pharmacodynamic marker of your drug effect on the disease process, you plateau out.
You get a pretty consistent effect across patients, and it isn't necessarily going to correlate. It's just telling you that the drug is doing exactly what it's going to do. What that translates into clinical effect is going to be kind of different from patient to patient, depending on their kind of context and how they fit in, if that makes sense.
No, that's very detailed and very helpful. Thank you. Just to recap quickly on the regulatory front, we just wanted to get a sense of when you anticipate sort of being able to provide us with the formal FDA stance.
It'll be sometime after we meet with them, and our plan at this point is to meet with the FDA within the fourth quarter. We can't be more specific than that at this point.
Thank you.
The next question is from the line of Boobalan Pachaiyappan with Roth Capital . Please proceed with your questions.
Hi, team. Congratulations on the progress. I'm dialing in for Boobalan, and we have a couple of questions. Given there is no FDA-approved therapy for DLB, can you provide a high-level feedback that you have received at the AAIC conference regarding the neflamapimod's week 32 data? What piece of today's data were the conference attendees most excited about?
I can't give you a general answer because most of the data was presented in a poster session yesterday. It wasn't an open oral presentation. I can just say that I was there and the people who came by, all the discussion was very, very positive. I think it's exactly as we are seeing it. This is a response that for the demonstration of clinical progression, the 16 weeks is a good result. Being able to show that over 32 weeks with the numbers and the robustness of the statistics, etc., is a great result. Everyone who saw that looked at it said this is very exciting. The GFAP data was, and we didn't present at AAIC because you have to have the posters actually up on the virtual site a couple of weeks ago.
GFAP data trails CDR Sum of Boxes inherently because the lab has to actually receive the samples, has to run process samples, get the data back to us. We just recently got the data, analyzed the data, and we're putting it out now because I think this is really, this is a material result. It has a, it's a, and the people who have seen that data are that much more excited because it's really just, you just tie it back into mechanism and effect on underlying disease process. As I said in my prepared remarks, it just is unambiguous evidence to when you put it together of proof of concept of a drug in DLB that acts on the underlying disease process to slow clinical progression. Everyone who's seen it is as excited as we are about it.
When will you disclose the full analysis, including the attention TUG and the ISLT scores?
We have the ISLT, all the other secondary endpoints, and this goes even to the 16-week data point. What distinguishes CDR Sum of Boxes from all the other endpoints is that it is the one endpoint that shows worsening, showed worsening in the placebo group over 16 weeks, shows consistently in phase IIa and this study, it's the endpoint that shows worsening. All the other endpoints, and the CGIC also inherently shows worsening, but all the other specific endpoints are flat. It's just within a 16-week period or 32, you need fundamentally, you need much higher numbers to see effects on that because in your control arm, you don't have worsening.
In the end, in the 16-week trial to see the effect on fluctuations and working memory with the ISLT recognition, this is clear-cut evidence of, or it's more evidence of the robustness and potency of the drug effect to be able to pick that up. At that time point, we had many more patients, and we had two time points. It was an MMRM analysis, and having two time points when you don't have worsening, it's the only way you can manage the variability. If you go up to the 32-week endpoint now, we're not going to have two time points, and the number in the extension of the 13-week study was a very small number. Nearly all the patients went on to new capsules eventually. There's no reason to look at that data or to present that data. It doesn't add anything.
I think for those endpoints, the 16-week data is informative, and it tells you what it is. The effect we're seeing here is a durability and sustained effect on clinical progression. When you don't have clinical progression on these other endpoints, you can't make that statement with a longer-term treatment.
Okay. One last question. Can you discuss the impact of neflamapimod old capsules on GFAP levels?
There's no effect on GFAP levels with the old capsules. During the placebo-controlled phase, placebo and old capsule GFAP both show a slight increase, and there's no significant difference between the two. This actually, in many ways, is more an objective biological confirmation that the old capsules were subtherapeutic. They're not pharmacologically active in the end because of the blood levels that they achieved.
Thank you so much, and congratulations on the progress.
Thank you. Yes, we are. Thank you. Again, I can't, it's the, we're very excited by these results. They're very consistent with the prior results, but to be able to go out to 32 weeks and showing the durable effect, which is associated with now a significant reduction in GFAP levels, and everyone who's seen this data from the academic community is highly impressed and quite excited.
Thank you.
At this time, I'll turn the floor back to management for any closing remarks.
Bill, do you want to close?
Yeah, I don't think there's much more to say. Thank you all for joining. As John just said, we're extremely excited about this data, as well as what we have ahead of us, and hope that everyone will continue to follow along and support.
Thank you. This will conclude today's conference. I'm going to disconnect your lines at this time. We thank you for your participation. Have a wonderful day.