Good afternoon and welcome to the ProMIS Neurosciences third quarter 2026 financial results and corporate update conference call. At this time, all participants are in a listen-only mode. Following the prepared remarks, we will conduct a question-and-answer session. As a reminder, this call is being recorded. I would now like to turn the call over to Carie Pierce, Vice President of Investor Relations and External Affairs. Please go ahead.
Thank you, operator, and good afternoon, everyone. Earlier today, ProMIS issued a press release announcing our financial results for the third quarter ended September 30, 2026, and provided a corporate update. The press release is available on the Investor section of our website and on our quarterly report on Form 10-Q and has been filed with the SEC and on SEDAR+. Joining me on today's call are Neil Warma, our President and Chief Executive Officer, who will deliver our prepared remarks, and Dr. Larry Altstiel, our Chief Medical Officer, who will be available during the Q&A session. Before we begin, I would like to remind everyone that today's call will include forward-looking statements with the meaning of the Private Securities Litigation Reform Act of 1995 and applicable Canadian securities laws.
These include, among others, statements regarding our clinical development plan and timelines for PMN310 and other product candidates, the interpretation and significance of the blinded interim data from our PRECISE-AD trial, our expectations regarding future clinical results, including the timing of top-line data, our financial position and cash runway, and our overall business strategy. These statements are based on management's current expectations and are subject to risks and uncertainties that could differ from actual results materially, including the risk that early or interim results may not be indicative of final or top-line results. Please refer to the Risk Factor section in our most annual report on Form 10-K and our subsequent filings with the SEC, including our quarterly report on Form 10-Q for the quarter ended September 30, 2026.
These statements speak as of today, November 12, 2026, and we undertake no obligation to update them except as required by law. With that, I will turn the call over to Neil.
Thank you, Carie. Good afternoon, everybody, and thank you for joining. ProMIS is entering probably the most important period in its history. Our phase I-B study, PRECISE-AD, in Alzheimer's disease is nearing completion. All patient visits are expected to conclude this quarter, and unblinded 12-month top-line data remain on track for the first quarter of 2027. Today, I want to focus on four things: why recent events in the field sharpen rather than weaken the case for PMN310, the strength of the interim data from July that we have seen in our PRECISE-AD trial, how we will judge the top-line results coming shortly, and how we are positioned both strategically and financially to move efficiently once we have the data. First, I want to directly address the phase II results reported two weeks ago by another company developing an antibody described as oligomer selective.
That trial did not meet its primary or secondary endpoints at 18 months. We have looked closely at the limited data that were disclosed, and two key findings really stand out to us. First, that the antibody produced statistically significant reductions in amyloid plaque on PET at both doses. Second, approximately 10% of treated patients developed ARIA-E, or brain swelling. In our view, both of those findings indicate meaningful engagement of plaque and fibrillar amyloid, not selective targeting of oligomers. That matters. A molecule that clears plaque and causes ARIA is behaving much like the existing plaque-directed drugs. So in our view, that trial did not test the oligomer hypothesis. Selectivity is not a label. It has to be demonstrated both at the bench and in patients. This is precisely where we believe PMN310 is different, and the data we have to date support that view.
The field still needs a clinical test of oligomer-selective targeting. We believe PRECISE-AD will be that test. Let me explain a little what sets PMN310 apart. PMN310, our lead candidate, our lead antibody, was built around one hypothesis, that toxic Amyloid-beta oligomers drive neurodegeneration in Alzheimer's disease, and that selective neutralizing and clearing them can deliver benefit without the safety burden of plaque-directed therapies. Three key features set PMN310 apart. Number one, selectivity. In head-to-head preclinical studies, PMN310 was the only antibody tested that bound toxic oligomers while avoiding monomers, avoiding fibrils, and avoiding plaque. Other antibodies include those described as oligomer selective, consistently showed binding to plaque. Additionally, the interim results from our phase I-B study presented last July, or this past July, have reaffirmed our confidence in PMN310's selective profile. Number two is design.
Like the two approved antibodies, PMN310 is built on an IgG1 backbone to engage microglia and actively clear toxic oligomers from the brain. We deliberately chose both neutralization and clearance. Number three is safety. By avoiding plaque, PMN310 is designed to reduce the risk of ARIA, which is still the single greatest barrier to the broader use of anti-amyloid therapy. At our six-month interim analysis, PRECISE-AD showed no ARIA-E, zero cases of ARIA-E in any APOE genotype. That's meaningful because with the approved antibodies, most ARIA occurs within the first six months of treatment. Though the interim read, to be clear, is not definitive, but it gives us real confidence going forward. The burden of ARIA goes beyond the brain swelling and bleeding it causes. To monitor for it, patients on the approved therapies must undergo as many as six MRI scans in their first year of treatment.
Keep in mind, these are cognitively impaired patients, and every scan is a real physical and financial burden on them, their caregivers, and the healthcare system. Our goal with PMN310 is to reduce the incidence of ARIA, and with it, dramatically reduce the need for repeated MRI monitoring. Should PMN310 deliver ARIA rates at or near placebo, with efficacy at least as comparable to existing therapies, we believe it could become a leading treatment for early Alzheimer's disease, and even open the door to preclinical asymptomatic patients where safety is absolutely paramount. Just as a reminder to the audience, the blinded six-month interim analysis of 136 patients, randomized 3:1 active to placebo, that we reported July 28th of this year, gave us an encouraging early read. There were no ARIA-E cases in any APOE genotype as of our cutoff date.
ARIA-H, a rate of 4.4%, all mild and asymptomatic, very much in line with placebo rates. There were no drug-related discontinuations, no treatment-related serious adverse events. On the target engagement potential drug effect side, we demonstrated pooled plasma p-tau217 decreased approximately 15% from baseline, and CSF MTBR-tau243 decreased approximately 13% from baseline. Remember, these are blinded pooled observations and not a determination of efficacy, but they are consistent with target engagement, and the safety profile is what we would expect from a true oligomer-selective antibody. Although no head-to-head studies have been conducted, our interim safety profile really stands in clear contrast to the ARIA-E rates seen in the recent competitor trial, and also with approved therapies. Let me turn to what we would consider a win when the top-line data read out in Q1 next year.
Every Alzheimer's therapy is ultimately judged on its balance of benefit and risk, as weighed by the FDA, by prescribing physicians, by patients, and their families. Today, that balance is a difficult one. The approved antibodies offer a modest slowing of decline at the cost of ARIA risk and an intensive MRI schedule. Our goal is to shift that balance decisively. PMN310 is designed to do that by lowering the risk side of the balance while preserving the benefit. Efficacy comparable to the approved therapies with a clear safety advantage would shift it meaningfully. Any efficacy above what we see with the marketed drugs would shift it even further. At top line, we will evaluate the totality of the data against that goal, really looking at four things. With respect to safety, we're looking for ARIA, drug-related adverse events, event rates approaching or comparable to placebo rates.
Clinical efficacy, we want to see a directional slowing of decline on either the iADRS or CDR Sum of Boxes versus placebo, so similar to approved therapies at the 12-months time point. Biomarkers, we would like to see changes that align with PMN310's oligomer-targeted mechanism, so directional trends in line with our oligomer selectivity mechanism of action. With respect to mechanism of action, we would like to show direct changes in oligomer levels following treatment with PMN310. If PRECISE-AD, if our clinical trial demonstrates a material shift in the benefit-risk profile, we believe it would be a significant value-creating event for ProMIS and a very meaningful step forward for patients. I want to take a minute now just to talk about how we are preparing for what comes next. We're not waiting.
We're not sitting and waiting for top-line data to come to plan the next phase. With fast-track designation already in hand, we intend to request a meeting with FDA after the full set of data is analyzed. In parallel, we're developing a subQ formulation of PMN310 and preparing for a potential registration study, which we could envision beginning towards the end of 2027, subject to FDA feedback, of course. We have also strengthened the team for that next phase. As we reported on October 5, Dr. Ivana Rubino has joined the ProMIS team as Chief Commercial Officer. Ivana brings more than 15 years of global neuroscience and Alzheimer's leadership from senior roles at Biogen and at Roche, and she will help shape our regulatory, late-stage development, and commercial strategy. Attracting someone of Ivana's caliber, I think, speaks volumes to the potential of PMN310 and our overall platform.
On that note, while we have a strong pipeline of selective antibodies for other serious neurodegenerative diseases with high unmet medical need, and this includes ALS, Parkinson's disease, dementia with Lewy bodies, I have focused today's call on our commitment to the Alzheimer's patients and their caregivers, and really around the enthusiasm we have for PMN310 and the upcoming data release. Before we kind of jump into a few questions and answers, I just want to turn briefly to our financial results for the quarter. We ended Q3 with approximately $44.1 million in cash, which we expect to fund operations through 2027, well beyond the PRECISE-AD readout. You can find full details of our financials in our press release and our Form 10-Q that was filed today.
Research and development expenses were approximately $6.7 million, down 32% from the $9.8 million from a year ago. The decrease was really driven by a $3.6 million reduction in direct PMN310 costs as the PRECISE-AD trial moved towards completion, and this is partially offset by more activity in our ALS and pipeline programs. G&A, general administrative expenses, were approximately $1.9 million, which was roughly flat with the $2 million from last year. Other income rose about $0.5 million from $0.2 million on higher interest income. Net loss overall for the quarter was $8.2 million, or $0.89 per share, and that's compared with $11.6 million, or $5.93 per share from a year ago. For the first nine months, net loss was roughly $28.1 million, or $3.39 per share, versus $29 million, or $19.58 per share in 2025.
Just before we jump into the Q&A, just to summarize, recent events in the field had really made one thing more clear. Targeting oligomers is only as meaningful as the selectivity behind it. PMN310 was designed for that selectivity, and our interim data to date, in the lab and in patients, fully support our hypothesis. We have encouraging interim safety and biomarker data, a strengthened leadership team, and a balance sheet that funds us through 2027. Our next catalyst is unblinded 12-month top-line data from the PRECISE-AD trial, expected in the first quarter of 2027. The question it will answer is whether PMN310 shifts the benefit-risk balance in favor of patients with Alzheimer's disease. On that note, I'm now joined, many of you know our Chief Medical Officer, Dr. Larry Altstiel. So I'm joined by Larry to answer questions coming through from the audience.
Operator, I would like you to please open the line, and Larry and I will take questions from the group.
Thank you. We will now be conducting a question-and-answer session. If you would like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star key. Thank you. Our first question comes from the line of Yatin Suneja with Guggenheim. Please go ahead.
Thank you for taking my question and going through the update. Neil, I think you just started talking or recently have started talking about what constitute a signal on the efficacy front. In fact, you have that also in the deck. It would be great to maybe talk about that a little bit. Also put in perspective the size of the study you are running relative to what we have seen in much larger study. I think it would be good for our investor to sort of understand that dynamic as well. Thanks.
Yeah, of course. Thanks, Yatin. Thank you for the question. Yeah, it's interesting. We do obviously get questions around expectations around the trial. I kind of hinted that in the script here in talking through it, but what constitutes, what's our target goal here with the PRECISE-AD trial? As I mentioned here, we're really focused on the benefit-risk profile. I do not mean to overemphasize that, but it really is important looking at both the risk side of the equation, so the safety versus the benefit side or the efficacy. From our goal here, as we just went through, is to shift or alter meaningfully that benefit-risk profile.
Our expectations in this trial, and as I think we said before, the best decision we made was in the design of this trial, and Dr. Altstiel sitting beside me is responsible for that, in a good way, a very comprehensive phase I-B study. Again, although it is comprehensive, it is I-B, we are looking at multiple endpoints with respect to biomarker safety, clinical outcome measures, and even mechanism of action around the oligomer reductions. We want to emphasize as well that this is a 140-patient study over 12 months, so direct comparisons with the larger 18-month study in 1,500 patients, we have to be careful putting that into context.
But I think for us, for expectations coming out the other side of this trial in Q1, if we could see safety approaching or close to that kind of background or placebo rate, especially around the ARIA-E, the burden of ARIA, as we mentioned, to patients and caregivers is significant. That really, as we said, is the single most thing restricting the uptake of the marketed drugs. We have heard this from prescribing physicians, we have heard this from pharma companies. If we, with PMN310, can dramatically alter the safety profile, reduce ARIA levels at or close to placebo or background rates, that would be a significant win. On the other side of the equation with the benefit, the efficacy, if we could at least maintain similar efficacy.
When kind of looking at some of those numbers, and again, we want to be careful here, but looking roughly at the efficacy numbers from the 18-month study, if you look at that 22%-27%, if we kind of back that up to 12 months, and again, careful how we put this into context, if we saw an efficacy rate kind of in the range of roughly 15%-20%, so similar efficacy to what we are seeing with marketed drugs, with a significant better safety profile, that we feel would be a significant win, and that is what we are hearing. Then any benefit kind of above that 20% would be total upside. We are trying to look at similar-ish efficacy with a much improved safety profile, and I think that would be a significant win.
If we saw that on the efficacy side as well, we would like to see directional trends in key biomarkers. I think the movement in the biomarkers, the trends we would see in some of these key biomarkers would tell us why we are seeing the efficacy in the clinical outcome measures. The clinical outcome measures that are important to us would be either/or the CDR Sum of Boxes or the iADRS. These are the FDA-approved endpoints. That, again, that range in that 15%-20% either/or iADRS or CDR Sum of Boxes, supported by directional trends in key biomarkers, which would really support the oligomer targeting thesis, together with a much improved safety profile with ARIA rates at or close to placebo.
Really helpful context. Thank you so much.
Thank you, Yatin.
Your next question comes from the line of Pete Stavropoulos with Cantor Fitzgerald. Please go ahead.
Hey, good afternoon, Neil and Larry, and thank you for taking my question. First question, part of it is sort of theoretical, but it would be great to hear your perspective. You do have these oligomers. They vary in molecular weight and size, consisting of the same fragments. Does binding them necessarily mean neutralization? Can you speculate if antibody-bound oligomer could still have neurotoxic effects? Then sort of tying that back to the question of how much of an impact can the Fc isotype make, especially IgG1 versus IgG2? Thanks.
Okay, thanks, Pete. It is a really interesting question. Does binding necessarily mean neutralization? I think that we have some hint from this from some of our preclinical studies in transgenic mice, where treatment with PMN310 actually preserved memory acquisition and memory retrieval, and also reduced the amount of inflammatory cytokines that were produced in the brain compared to placebo. That does tell us, gives us at least a hint, that neutralizing the antibodies does have some effect in terms of activity. Now, can the antibody-bound antibody actually still have, or antigen-antibody complex still have toxic effect? I think the answer to that is unknown, but I do think that the antibody can stabilize the toxic oligomers and render them less toxic.
However, if there is some ambiguity there, that really does speak to the importance of the IgG1 background, because even if there is residual toxicity of the antigen-antibody complex, that removal ablates that effect. That really does speak to the importance of what we have done here, of having a very highly specific antibody that has a really, really low KD. That means that it really binds to it, hangs onto that oligomer, and does not let go, and then it is bound and removed by microglia. I think that they both work in concert that way.
All right. Thank you very much.
Your next question comes from the line of Keay Nakae with Chardan. Please go ahead.
Yeah, thank you. Appreciating that your data is going to be at 12 months, and there is some interpolation there. Does the shape of the curve at 12 and the degree of separation, how much does that also impact your Go/No-Go decision?
Yeah, I think it needs to be looked at kind of collectively, Keay. Thanks for the question. Again, we are looking at it across the various kind of baskets of endpoints, if you will. If we see, again, it is 140 patients, 3:1 randomized, I keep referencing that. I think if we see that benefit coming in that range that we are saying, the separation we see between active and placebo, combined with directional trends in those key biomarkers, I think that will be kind of a really important signal. Again, we have also got, safety is going to drive a lot of this as well. Then I think we sit with the FDA.
Again, we plan with our end of phase II meeting once we collect all the data, and we sit with them, and we work with the FDA to demonstrate the benefit-risk profile that we are taking forward, the rationale around reducing significantly, we feel, the number of MRIs that were required. We have also got our mechanism of action data. Again, for the first time, we have got the assay that allows us to measure and detect levels of oligomers, and their reduction with PMN310. I think if you put those data points together and really showcase that benefit-risk change, then FDA should be in favor of allowing us to move forward with that next, ideally, registrational study.
Okay. Just, if I could ask a follow-up on the subQ, how confident are you, based on any PK data you have, that you will be able to formulate something equivalent, and how soon might that be ready? Will that be what you use in the pivotal?
Yeah, it's a good question. Our goal is, I think, as we've said, over the past few months now, we really initiated that subQ development program around the time of the interim analysis. I think we were certainly given confidence by the interim data, enough to pull the trigger to get the formulation around subQ going forward. It is our goal to bring the product to market as a subQ product. We're looking to where the market's evolving to and where it will have evolved in the next few years. SubQ is going to be important if we come to the market with that benefit-risk much improved. We want to be there with a very patient-compliant product as well. The early studies we've been working on are encouraging.
Obviously, a lot's going to depend on the results from the study around dose, but the PK that we're looking at early studies, the viscosity, the volumes required for subQ and making it manageable and painless for the patient are all going well. Our goal then is to, once we get into that next, ideally, the registration study, we would see ourselves running a subQ arm within that larger study. This would be, we're not going to slow down IV to let subQ catch up. No, Larry, it'll be a combined.
Yeah. I think, when you talk about PK, one of the things we'd like to get from the phase I-B study is a dose and exposure that gives us a maximum effect with respect to efficacy, safety, and biomarkers. That would be an initial benchmark. By running the subQ formulation equivalency studies alongside phase III, we've got a comparator arm so that we know what we have to hit with the subQ.
Yeah.
We're not slowing down the IV formulation, no, far from it. I think the subQ formulation will be able to catch up, especially because we have these normative data from the phase III study.
Yeah, so it is looking good, and it is, as I said, it is our goal to get to market with the subQ, for sure.
Great. Thank you.
Thanks, Keay.
Your next question comes from the line of Fozia Ahmed with Brookline Capital Markets. Please go ahead.
Hi, teams. Thank you for taking my question. My first question is, with the upcoming CTAD presentation focused on the six-month interim safety and biomarkers finding, could you give us some sense whether there will be additional insights from the data, or it will just be the similar, what we know that was disclosed in July?
Hey, Fozia. Yeah, thanks for joining. Thanks for the question. It will be, yeah, no additional information at CTAD. I mean, our goal at CTAD, as you rightfully say, is coming next week, when we are all there. We are presenting a poster which represents the interim analysis from last July. I think our goal there is just to continue to remind people of the differentiation of PMN310, remind them of the data that has been generated to date, including the interim analysis from a couple of months ago, remind them of the data that is coming up in a few months. So, it is really to kind of increase our exposure. We are reaching out very much at clinical KOL-driven events. We have got a number of interactions with KOLs, number of interactions with strategics and pharma companies.
It really is a way just to kind of reinforce our differentiation as a- I will not say the only, but certainly, in our view, one of the more exciting next-generation anti-amyloid therapies company, anti-amyloid drugs coming along. So it is very much kind of getting out in front of some of the KOLs and clinicians and pharma companies. But again, no new data will be presented on our part.
I think there will be probably some contextual interest here, given the results with ACU193. So we will be able to kind of reemphasize what we have had accomplished at the interim.
Thank you. I have one follow-up. Given that toxic oligomers are structurally heterogeneous and they keep changing conformation, can you share some thoughts on how PMN310, we know it recognizes a very specific conformation or specific epitope on that conformation. As these oligomers are changing, how accessible that epitope is to PMN310?
Yeah, I think when the epitope is exposed, that is kind of a definition, in fact, of the toxic oligomers. As you point out, they are very plastic, poorly structured, and the epitope does appear on these. But as they become more structured and less toxic, that epitope is buried inside fibrillar structures, high-order fibrils, and ultimately in plaque. So really, it is almost definitional that the aggregates of A-beta peptide that display this epitope do represent probably the bulk of the toxic oligomers that we are trying to eliminate.
Mm-hmm. They are consistent across kind of all brains and Alzheimer's brains we have tested, hundreds.
Yeah.
That binding, that conformational epitope is consistent across all Alzheimer's brains.
Yeah, and of course, it's not just one patient or a handful of patients. Also, too, looking at low molecular weight fragments of brain homogenates are enhanced in oligomers. PMN310 removes the bulk of the oligomeric material there.
Perfect. Thank you so much.
Thanks, Fozia.
Thanks, Fozia.
Your next question comes from the line of Boobalan Pachaiyappan with Roth. Please go ahead.
Hi, this is Aaron on for Boobalan. I just wanted to ask a question about Acumen's reported CSF antibody oligomer engagement was assayed before by your company. I wanted to know what kind of oligomer binding differences, oligomer species binding differences you detected that may explain some of the clinical differences that have been observed, and if you will be reporting on any of these readouts in the oligomer species and free oligomers or antibody-bound complexes in the readout later in 2027.
I think that the Acumen binding assay really represented an antibody saturation assay, and the antibody being saturated with whatever PMN310 or ACU193 binds, oligomers and a lot of other stuff as well. Our assay is quite a bit different in that it measures the absolute concentrations of A-beta oligomers themselves. It is not inferential with respect to antibody saturation, but rather, it measures the absolute concentration of oligomers in the cerebrospinal fluid. We demonstrated this, it was disclosed in a poster earlier this year at AAIC, and it's, to the best of our knowledge, the first time that anybody's ever been able to do this with this sort of sub-picomolar kind of sensitivity that's required to detect not only the oligomers, but also, in our particular case, a dose response in a single dose phase I study.
That's what we'll be reporting, is the absolute decrement or change in oligomers as opposed to an antibody saturation.
Mm-hmm. Yeah, that is why I kind of, thanks for the question, Aaron. It is exciting for us. As Larry said, for the first time, we will be able to kind of show, hopefully to prove our mechanism of action or our hypothesis that we have got an antibody that binds and clears oligomers. Up until now, we have never had an assay, no one has had an assay that was sensitive enough to measure this low concentration of oligomers. Again, importantly, if we can show the safety, biomarker movement, clinical outcome measures, and we can show precisely that it is due to the mechanism that we have proposed, that will be very, very interesting, not only for FDA, but also for us and pharma companies going forward if we can connect the mechanism of action. We are excited to be able to present those data.
That assay, as Larry said, is being implemented into the phase I-B trial. We will look at pre and post-treatment of oligomer levels with PMN310.
Great. Thank you, guys.
Thanks.
Your next question comes from the line of Raghuram Selvaraju with H.C. Wainwright. Please go ahead.
Hi, Larry. This is Jade on for Ram. Thanks for taking our question.
Hi, Jade.
Hi, Jade.
Hi. You've previously discussed the potential for substantially less frequent MRI monitoring. The question is, how and when would you evaluate whether this reduced schedule is appropriate, particularly in the APOE4 homozygotes?
Well, right now, to date, we have seen, or at least not to date, but in the six months of analysis, we haven't seen any ARIA-E. And we have the normal distribution that one would expect with APOE genotypes in an Alzheimer's population. So there were a number of APOE4 homozygotes, a high degree of APOE4 heterozygotes. And again, we saw no ARIA-E in this population and an ARIA-H rate that was consistent with what one would expect to see in an untreated patient population, just the natural history. With respect to how many MRI scans will be required as per the label, that's a discussion that we have to have with the agency, and we can't really predict that they will say, "No more MRIs." We will just simply present the evidence as we have it to date, and then as it accrues in subsequent studies.
I think if we see the same sort of trend, I think that we'll be able to get rid of much of the MRI surveillance early on in the study.
Yeah. Importantly too, Jade, I believe that when you look at trontinemab, that's using a shuttle here, and they've reduced their ARIA incidents significantly with the shuttle. Of course, shuttles bring their own complications. But interestingly, I believe in their phase III design, the agency has reduced the number of MRIs that they're allowed from five or six down to three. So there's precedence coming from the FDA that if you can reduce. I think it's important because we've been asked, is this a class effect, and as an anti-amyloid targeting agent, regardless of ARIA, you're going to be given the same whack on the wrists that lecanemab and aducanumab found. I don't think that's the case, and I think trontinemab shows that it's not a class effect.
If we can come with an even cleaner safety profile, then there's a good chance that the MRI burden will be significantly reduced, ideally in the next registration study that we want to run. If we can consistently show low levels of ARIA going forward, we would expect that come launch time.
It's not going to be on the label.
it's not going to be on the label, which is important. I think there's good signs that we can dramatically reduce the MRI, because as I said in the piece earlier, it really is so cumbersome, burdensome for these patients and their caregivers to go multiple times a year for an MRI. You can imagine putting some of these patients who are not feeling too well into an MRI machine multiple times a year is horrible. Ideally, that's one of our goals, and I think that in addition to saving on costs and healthcare costs, the burden for the patient will be significantly reduced.
Well, as Neil pointed out, there is FDA precedent that we've seen that when you have the appropriate data, FDA will make a data-driven decision and say, "The data suggests that you don't need all these scans." We think that we'll come in with a safety data package that we'll present to the FDA. I'm not going to presume what they will say, but we do have the precedent that they are flexible about eliminating this apparent class effect and having a data-driven outcome.
Great. Thank you so much. Just quickly, I was trying to find the participant number for the plasma p-tau217 and the CSF MTBR-tau243 charts in the presentation, and I wasn't able to find them. Could you tell me?
Yeah, we didn't provide. These are kind of when all patients, the total number of patients enrolled was 144. The safety evaluable number was 136. When all those patients had reached the six-month level, that's when we did our safety and biomarker analysis. We didn't give specific numbers on MTBR or p-tau as far as how many numbers of samples were collected from the patients. We didn't break that out in kind of finite detail. We'll do all this kind of at the end of the study. We'll put all the patients and all the unblinded data, but we didn't communicate that at the interim level.
Okay, great. Thanks so much. Looking forward to it.
Yeah, thanks. Thank you.
Your next question comes from the line of Pete Stavropoulos with Cantor Fitzgerald. Please go ahead.
Yeah, thank you for taking my follow-up. Assuming a positive outcome for the phase I-B, and I understand that you need regulatory interactions, but how are you currently thinking about next steps? Are you leaning towards a phase II-B, a phase III, or perhaps a phase II/III adaptive design, and what will drive that decision? Thank you.
Yeah, thanks, Pete. That's a good question. We're doing a lot of that discussion now, and obviously bringing somebody like Dr. Ivana Rubino onto the team allows us to think a little bit more deeply, comprehensively around those questions. I think for us, it could be our thinking is kind of a registrational type study, whether that's a phase III or II/III adaptive. We'll see what kind of the data will dictate some of that. We're doing those kind of design elements now, kind of including a subQ arm, as we talked about earlier. I think for us, we're being pretty bullish on single registration study. The exact size and shape and cost we're working on now. We haven't really given any guidance. I think we'll use Dr. Ivana Rubino's expertise, Larry's expertise, to continue to think through various approaches.
What we are doing, taking advantage of this wave and enthusiasm around AI, and we're careful how we do that, but there's a lot of input we're getting from AI, or we will get from AI, around clinical trial designs, improving efficiency, and cost reduction. There's a number of elements we're building into the design perspective. I think as we go forward, get the data, sit down with the agency, and get their feedback, that will kind of shape our final decision.
Yeah, I think, Pete, I wouldn't dwell too much on whether we call it a phase II-B, phase III, or II/III, but rather focus on a clinical trial that's going to stand as a registration-quality study.
Yeah.
Now, there's a lot of different ways to get there, and as Neil pointed out, we're exploring them as we speak. But that's our goal.
Yeah. Again, keep in mind, the reason we designed such a comprehensive I-B study was to be able to step into a registrational-type study. As I said, we were pretty aggressive in numbers and length of treatment in order to kind of speed time to market and ideally get in front of the agency and propose a registration study that gets us to commercial stage quicker than if we had done a smaller I-B study. We're pleased with the design, and ideally, the outcome will dictate a lot of things in a few months.
Great. Thank you for that, and looking forward to the data in Q1.
Very good.
Thank you.
Thank you much, Pete.
This now concludes our question-and-answer session. I would like to turn the floor back over to Neil for closing comments.
Yeah. Thanks, Kate, very much for your support. And thank you, everybody, for your time and your questions today. As I said, our focus really remains on patients and their families, and we are looking forward to showing in a few months that PMN310 could change the benefit-risk balance in Alzheimer's disease and really help the patients who so urgently need it. So thank you so much for your attention and your support. We will update again soon.
Ladies and gentlemen, thank you for your participation. This does conclude today's teleconference. You may disconnect your lines, and have a wonderful day.