On Thursday, ProMIS Neurosciences (NASDAQ:PMN) discussed second-quarter financial results during its earnings call. The full transcript is provided below.
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Summary
ProMIS Neurosciences reported positive interim data from its Phase 1b Precise AD trial for PMN310, showcasing a favorable safety profile with no cases of ARIA-E and early biomarker improvements.
The company ended the second quarter with $53.4 million in cash, ensuring it can fund operations through 2027, covering the anticipated top-line readout of the Phase 1 trial.
ProMIS is advancing its broader pipeline, including PMN267 for ALS and PMN442 for synucleinopathies, with both candidates progressing toward IND-enabling studies.
The company is exploring a subcutaneous formulation of PMN310 to enhance patient compliance and market reach.
Management expressed confidence in PMN310's differentiated safety profile and potential efficacy, positioning it well for future regulatory and market opportunities.
Full Transcript
Carrie, Investor Relations
And issued a press release with our financial results. Both are available in the Investor Relations section of our website at promiseneurosciences.com. Before we begin, I would like to remind everyone that statements made on this call include forward-looking statements within the meaning of the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. These include, among others, statements regarding our clinical development plans and timelines for PMN310, PMN267 and our other product candidates, the interpretation of the significance of the blinded interim data from our Precise AD trial, our expectations regarding future clinical results and our financial position and cash runway, and our overall business strategy. These forward-looking statements are based on management's current expectations and are subject to risks and uncertainties that could cause actual results to differ materially from those expressed or implied. We encourage you to review the risk factors described in our most recent Annual Report on Form 10-K, our Form 10-Q filed today, and other filings with the SEC.
We undertake no obligation to update or revise any forward-looking statements as a result of new information, future events or otherwise, except as required by law. With that, I would like to turn the call over to Neil.
Neil
Thank you, Carrie. Welcome to all those who are joining us today to discuss ProMIS Neurosciences' results for the second quarter of 2026 and also to review the recent progress across our pipeline. As Carrie said, joining on the call today is Dr. Larry Altstiel, our Chief Medical Officer, who will walk us through the encouraging interim data we recently reported from our Phase 1b Precise AD clinical trial. I'll then provide a financial update before we open the line up for a few questions.
As many of you know, ProMIS is a clinical-stage biotechnology company applying our patented technology platform to build a portfolio of antibody therapies and therapeutic vaccines for neurodegenerative diseases with a focus on Alzheimer's disease, dementia with Lewy bodies, ALS and Parkinson's. We believe these diseases share a common biological cause: normal proteins that misfold become toxic and kill neurons. Our platform is designed to combine protein biology, physics and supercomputing to selectively target these toxic misfolded proteins while sparing their healthy, properly folded counterparts.
Our lead product candidate is PMN310, which is a monoclonal antibody designed to treat Alzheimer's disease by selectively targeting toxic misfolded oligomers of amyloid beta. Behind PMN310, we are advancing PMN267 for ALS, which targets misfolded TDP-43, and PMN442 for synucleinopathies such as dementia with Lewy bodies and Parkinson's disease, which target pathogenic alpha-synuclein. Both PMN267 and 442 have been humanized in a human IgG1 framework and are advancing toward IND-enabling studies.
We're also progressing a set of vaccine programs in Alzheimer's and Parkinson's and ALS. As we've recently discussed, the second quarter was a defining period for ProMIS. In late July we reported positive blinded six-month interim safety and biomarker results from our ongoing Phase 1b Precise AD clinical study of PMN310, data we believe reinforce the core thesis behind our oligomer-selective approach. Larry will walk us through the details in a moment, but at a high level, the blinded interim analysis yielded a favorable safety profile across all participants and genotypes, showing no cases of ARIA-E, and early directionally consistent movement in two complementary biomarkers, plasma pTau217 and CSF MTBR-tau243, which is consistent with target engagement. We believe these data reinforce the central thesis behind PMN310: that by selectively targeting toxic amyloid beta oligomers rather than plaque, we have the potential to deliver the benefits of amyloid-directed therapy without the ARIA burden that has constrained this class of medicines. We actually hosted a live webinar back on July 28 with two independent key opinion leaders, Dr. Will Montai, University of Minnesota, and Dr. Mike Weiner of UCSF, who shared their perspective on the data and its clinical relevance. For those of you who missed it, the presentation and recording of the webinar are available archived on our website and this, we believe, is truly the most meaningful clinical milestone in the company's history to date. I would now like to ask Dr. Altstiel to walk through the Precise AD summary of the interim data in a little bit more detail.
Larry, if you would please.
Larry Altstiel, Chief Medical Officer
Thank you, Neil, and good afternoon, everyone. I'll walk through the six-month blinded interim data from Precise AD that we announced on July 28, starting with the trial design, then safety, then biomarkers, and close with what we expect as we move toward the 12-month top-line readout. Now, Precise AD is an ongoing Phase 1b trial of PMN310 in patients with mild cognitive impairment due to early Alzheimer's disease. It's a randomized, double-blind, placebo-controlled, multiple ascending dose study.
We completed enrollment in December 2025 with 144 subjects across 21 active sites in the United States, randomized 3 to 1 active drug versus placebo across three dose cohorts of 5, 10 and 20 mg/kg dosed monthly by IV infusion over 12 months. Of the 144 enrolled subjects, 136 were included in this interim safety analysis. This is a genetically and demographically representative population. Mean age was 73.3 years, 58% of patients were female, and importantly 61% of patients carried at least one APOE4 allele, with 11% being APOE4 homozygotes—that is the proportion at the very highest risk of ARIA with plaque-binding antibodies and one that is often underserved by approved amyloid-directed therapies today. As of the July 22 data cut-off date, all 136 safety-evaluable patients had been dosed for at least six months, 78% had passed nine months, and 49% had already completed the full 12 months of dosing. Safety was the primary focus of this interim look. Given that PMN310 was designed as a non–plaque-binding antibody with the goal of significantly reducing the ARIA risk, the results were encouraging.
We observed zero cases of ARIA-E, which is the more serious symptomatic form of ARIA involving brain swelling. This result was noted across all genotypes, including in the APOE4 homozygote population. Total ARIA, which includes the milder ARIA-H microhemorrhage finding, was 4.4%, and every case was mild and asymptomatic. We saw no treatment-related serious events and no drug-related discontinuations through the interim cut-off, and only one single non-serious infusion reaction—a rate notably lower than the infusion reaction rates reported for approved anti-amyloid therapies in their pivotal trials.
These are descriptive comparisons against published data and not head-to-head studies, but directionally this is a differentiated safety profile, particularly in the APOE4 carrier population where approved therapies today carry their most significant warning. Now with biomarkers, I want to frame this next part carefully because Precise AD remains a blinded ongoing trial, and these are early exploratory signals and are not efficacy readouts. We looked at two complementary biomarkers chosen to bracket different points in the Alzheimer's cascade: plasma pTau217, one of the earliest and best-validated biomarkers of amyloid-driven tau pathology; and CSF MTBR-tau243, a more downstream, tangle-specific marker that correlates closely with tau PET imaging and cognitive decline in untreated placebo-arm patients. From published natural history data, both markers are expected to rise over time as disease progresses. In our blinded pooled analysis—meaning this combines both drug- and placebo-treated patients under the 3-to-1 randomization—we saw the opposite: plasma pTau217 declined approximately 15% from baseline, and MTBR-tau243 declined by approximately 13.3%, with about 62.5% of patients showing a decline.
Both the direction and the proportion of patients showing a favorable response are broadly consistent with the trial's 75% active drug allocation. We think it's notable that both an upstream, amyloid-linked biomarker and a downstream, tangle-specific biomarker moved in the same favorable direction at the same time point. That consistency is encouraging, although again this remains a blinded interim look and it is not a determination of clinical efficacy.
The trial is ongoing and remains blinded. We anticipate all patients to complete their 12-month dosing by the fourth quarter of this year, and following database lock and statistical analysis, we expect to report unblinded 12-month top-line data in the first quarter of 2027. That readout will include the full safety dataset, a more detailed biomarker panel, and for the first time we will also report on clinical cognitive outcome measures, which will let us assess PMN310's efficacy in a controlled and unblinded setting.
And with that, I'll hand it back to Neil.
Neil
Thanks very much, Larry. Yeah, again a very kind of encouraging set of interim data. Thanks for the presentation. Beyond PMN310, as I touched on earlier, our broader pipeline continues to advance. PMN267, our program targeting misfolded TDP-43 in ALS, has been humanized in an IgG1 framework and is progressing towards IND-enabling studies. PMN442, our lead candidate for dementia with Lewy bodies and Parkinson's disease, potentially other synucleinopathies, has also been humanized and is advancing towards IND-enabling studies based on its selective binding to pathogenic alpha-synuclein.
And then behind those we continue to advance our vaccine program in Alzheimer's disease, ALS, and Parkinson's, and are further developing our EPI Select Discovery platform in which we are incorporating machine learning to accelerate identification of new disease-specific epitopes. Just turning to the financial results briefly for the quarter, we ended the second quarter with roughly $53.4 million in cash and short-term investments compared to $6.1 million as of December 31, 2025.
That increase primarily reflects the roughly $70.1 million in net proceeds we received in January 2026 from our private placement financing. Based on our current operating plan, we expect our existing cash and investments to be sufficient to fund operations through 2027, which importantly carries us through the anticipated 12-month top-line readout from our PRECISE-AD Phase 1 trial expected in the first quarter of 2027. For the second quarter we reported a net loss of roughly $11.7 million, which equates to $1.28 per share, compared to a net loss of roughly $10.1 million, or $7.26 per share, in the second quarter of 2025.
The improvement in loss per share reflects the increase in weighted average shares outstanding following our January financing. Research and development expenses were approximately $9.5 million for the quarter, up slightly from $8.7 million a year ago. General and administrative expenses were $2.7 million, up from $1.4 million, reflecting increased professional fees and headcount as we have modestly built out the infrastructure to support operating as a clinical-stage company.
For the first six months of 2026, we reported a net loss of roughly $20 million compared to $17.5 million in the prior-year period. R&D expenses were $16.5 million for the first half, up from $14.2 million, largely reflecting full enrollment and dosing activity in the PRECISE-AD trial. G&A expenses were roughly $4.4 million compared to $3.4 million a year ago. Net cash used in operating activities was roughly $22.8 million for the six months compared to $8.8 million in the year prior, consistent with the increased pace of our clinical activity.
A brief summary of the financial results. So to summarize in closing, this has, as we've laid out, really been a transformational quarter, a transformational year thus far for ProMIS Neurosciences. The blinded six-month interim data from the trial, we believe, provide the first human evidence supporting our oligomer-selective approach: a favorable safety profile with no ARIA-E across all genotypes, including a high proportion of APOE4 carriers, alongside early biomarker movement consistent with target engagement and a potential drug effect.
We believe these data speak directly to the potential of PMN310 to offer a differentiated safety and efficacy profile in Alzheimer's disease. We're well financed to reach our next major catalyst with a cash runway through 2027 that importantly spans the unblinded 12-month top-line readout expected in the first quarter of next year. And beyond PMN310 we continue to advance a deep and differentiated pipeline across Alzheimer's, ALS, multiple synucleinopathies, all powered by our EPI Select platform.
I want to take this time to thank, importantly, our patients, their families and all the caregivers, our clinical investigators, and our employees for their dedication, as well as our shareholders for their continued support. We look forward to keeping you updated as we approach these important milestones. Thank you so much for your attention. And operator, I think we're ready to take a few questions, please.
OPERATOR
Thank you. We will now begin the question-and-answer session. To ask a question, you may press star, then the one on your touchtone phone. To withdraw your question, press star, then two. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. First question comes from Yatin Suneja with Guggenheim Partners. Please go ahead.
Yatin Suneja, Analyst at Guggenheim Partners
Hey guys, thank you for taking my questions and nice progress. Congratulations on the recent result. So I have maybe three questions, if I may, one broader question and two specific questions. I'll ask the broader one first. So now that you've had some time to process the data, could you perhaps talk about the KOL reaction to these data and then what comes next for 310? And I'll ask the two other questions afterwards.
Neil
Thank you. Sure. Thanks, Shat. And thanks for the comments. Maybe I'll just touch on the first one, the KOL reaction and the investor reaction. Larry and I had a busy couple of weeks since the release of the data and I think overall the KOL, the overall reaction response has been very positive. I think we set expectations going into the interim analysis and we were careful how we set those expectations, and I think the data we saw from a company perspective, we certainly met our expectations and probably even exceeded them a little bit.
The safety was extremely encouraging. The target engagement signal was again encouraging as well. And I think this was reflected very much by the external stakeholder groups — the KOLs, the investors, the shareholders — all were quite buoyed by the interim data. So we were pleased with that. And I think that kind of reflected from the webinar, the two KOLs, the independent KOLs we had on our call were quite supportive of the data as it related to their neurology practice as well.
As far as what's next for PMN310 — and thanks for that question — we're certainly not just sitting and waiting for the data to read out in Q1. We're looking forward as to how we manage the lifecycle of PMN310 all the way to market. Contained within that internal program, if you will, is what potentially is the next clinical trial that follows this one if the data are successful. Larry and the team are working hard on designing the next clinical trial.
We believe that if the data are positive and continue to be positive and read out positively in the top line, we anticipate stepping into a single registration study. So the clinical development plan is certainly being refined for the next clinical study. The regulatory path — we expect meeting with the FDA; we do have Fast Track designation for this program — we expect meeting with the FDA shortly after the final data set together, so the regulatory path is important to us.
We're also developing or looking at developing a subcutaneous (sub-Q) formulation. Right now it's monthly IV dosing. Getting to market with a sub-Q formulation is very important to us, so that's also in the works as well. And then we're also looking — as Larry said, this patient population we're addressing now is that MCI, early Alzheimer's patients — there's a lot of interest in the asymptomatic preclinical AD patient population. So we're also looking at that expansion, or label expansion if you will, as to how we address that market, because we think having a product like PMN310 that ideally delivers better efficacy but importantly a much better safety profile, that preclinical AD population is one that we could address quite well with a very safe and effective product. So there's multiple prongs here that are being internally assessed and evaluated and prepared — really that lifecycle management for PMN310. In addition, obviously we're having discussions with strategics. There's a lot of interest from the pharma companies in what we're doing, so looking at how to work with them potentially in the future, or potentially looking at how to fund the next study ourselves.
So those strategic options are also part of the discussions internally.
Yatin Suneja, Analyst at Guggenheim Partners
Very good. That was excellent, Neil. Then perhaps the two follow-up questions. So one is on the biomarker and then the one is on the safety. So with regard to the biomarker, or the blinded biomarker, I understand I think you and Larry have emphasized that we should not be over-reading it at this stage. But to us, you know, the target engagement is pretty clear at least, or pretty evident, because we don't think there is any reason for pTau217 to decline in an untreated AD population.
So the question is how should we think about target engagement for 310? And then on the safety side, yes, I think it's very clean safety and tolerability. So the question is, with regard to ARIA-E, does it reflect the front-loaded class pattern, or does it hold beyond six months? Love your answer on both of those. Thank you.
Neil
Maybe I'll turn that over to Larry. Larry, if you want to speak on what we kind of feel about the target — I think we're pleased with the target engagement signal. Maybe you can speak a little to that and then to the safety as well, please.
Larry Altstiel, Chief Medical Officer
Yeah, I think we're pleased with the target engagement signal. Again, we were happy to see a robust decline in pTau217 really beginning at the first month and then continuing on and increasing up to six months. And as Neil pointed out, the natural history of pTau217, if it's unopposed by any sort of therapy, is to increase over that period of time, so we were happy with that result. And we were also happy with the pTau, the MTBR-tau243 result, because that really represents a form — you know, the onset of tauopathy.
And when tauopathy begins, that's really the onset of, you know, frank clinical decline. So we were happy with both of them. And because they bracket kind of two ends of pathology of oligomer-based pathology — that is, one, increasing tauopathy with pTau217 and then the increase in abnormal phosphorylation of tau going on to neurofibrillary tangles — we think that that's an interesting sign of potential target engagement. And now with the safety, the safety data were not really cut off at six months, but actually reflected the total safety data — which we review every day, by the way — up to the time of the interim analysis, which was July 22nd. And so a substantial number of patients had crossed the six-month threshold. Almost half of the patients had finished the study. So we think that, again, the absence of ARIA-E is certainly due to the fact that we engineered PMN310 to avoid amyloid plaque. It does not bind to amyloid plaque in the brain and also in the vasculature. So we think that that's principally the reason why we're not seeing any ARIA-E. And the ARIA-H data probably represents the baseline increase that you see in Alzheimer's patients due to cerebral amyloid angiopathy, and this is what is commonly seen in patients who are not being treated with drug — you'll see a small amount of ARIA-H that increases over time. So again, I think that with the ARIA we were quite gratified to see that signal. And then also, safety and tolerability don't really end with ARIA. We didn't see any serious adverse events related to drug therapy. We didn't see any dropouts related to treatment. And also the infusion reaction rate was actually quite low, with just simply one case of a mild infusion reaction that did not require change in dosing.
So all in all, I think that our impression is that the safety is really quite remarkable and that we do have evidence of target engagement.
Neil
And to your point also, Yatin, the importance of six months, I think, is also kind of emphasized when we know that the majority of ARIA cases, ARIA-E and ARIA-H, occur early. Certainly when you look at our graphs in our presentation, the majority—90 plus percent—of ARIA cases occur in the first six months of dosing. So to see zero cases in, as Larry said, six plus months—half the patients have actually completed 12 months of dosing—so it kind of goes beyond six months.
So again, that six-month threshold, when we know typically from the donanemab and lecanemab studies 90% of the cases occur, we're that much more pleased with our zero cases over the first six plus months.
Yatin Suneja, Analyst at Guggenheim Partners
Excellent, thank you.
Neil
No, thanks, John, for the questions. Operator, I think we can take a couple more.
OPERATOR
Next question. Pete Stavropoulos with Cantor Fitzgerald, please go ahead.
Pete Stavropoulos, Analyst at Cantor Fitzgerald
Yeah, hi, Neil and Larry, how are you? Congratulations on the updates and progress for the quarter, and thank you for taking our questions. One question is whether you have target engagement when dosing humans in PMN310? You did present some data at AAIC about a month ago. Can you talk about this assay and outcomes, and when can we expect to see a similar analysis for the Phase 1b? And will we get any additional biomarker data from the blinded interim look before the 1Q27 readout?
Larry Altstiel, Chief Medical Officer
Yeah, Pete, I think I'll start with your question and work backward. We'll have a much more fulsome presentation of all the biomarkers in the clinical trial along with the clinical outcomes when we unblind the data after the study is concluded. With respect to the assay that you were speaking about that we disclosed at AAIC, this is an assay to detect Aβ oligomers in cerebrospinal fluid. Now, the Aβ oligomers, although they are extraordinarily toxic, are present in very low concentrations, in picomolar concentrations—10 to the minus 12—so they're very hard to detect.
Other companies have used an antibody saturation approach to look at antibody saturation of them, but no one has really, to date, measured the exact thing itself, that is the Aβ oligomers. And I think what we showed here for the first time, in conjunction with our colleagues in Germany, was that we actually measured the concentrations of Aβ oligomers. And we did this in a Phase 1a study. These are participants who were otherwise healthy but nonetheless had low amounts of Aβ oligomers, and we were able to detect the dose response with that even after a single dose of PMN310.
This assay is still being refined, but we expect that it will be used, and we'll present the data again when the study is completed.
Neil
Yeah, I think the importance—and thanks for the question, Pete, and your comments—the importance of that assay, as Larry said, is really to elucidate the mechanism of action that we've been predicting, if you will, over the number of years since we've been developing PMN310, that being the binding to the oligomers and the removal of those oligomers. And as Larry said, that has not been possible because there's never been an assay sensitive enough to measure these oligomers.
So now that we've shown early data that we can indeed develop an assay that is sensitive enough to not only measure these oligomers, we also show that in the presence of PMN310 there is actual reduction of these oligomers from circulation. And again, this was done in our 1a samples, but it really is kind of connecting the dots around the mechanism of action. So this assay will be implemented into the Phase 1b study so that we can look at pretreatment and post-treatment results to see whether or not indeed we actually are able to reduce the level of these circulating oligomers.
And then ideally that lines up with the clinical evidence we see at the end of the study, and ideally with the biomarker evidence. So having that mechanism-of-action piece is significant for our own use, but certainly when it comes to regulatory authority approval as well. And there will be no unblinding or blinded data presentations prior to the final results coming out.
Pete Stavropoulos, Analyst at Cantor Fitzgerald
Okay, a couple of follow-ups. So, the current formulation in the Phase 1b is IV administered. How are you thinking about the potential subQ formulation? Is it feasible? Are you working on it? And what formulation would you actually like to bring forth, assuming the Phase 1b is positive?
Neil
Yeah, that's a good question. We touched on it a minute ago a little bit, but it's important to us to deliver the product to market in a subQ formulation. I think we're expecting to have improved efficacy versus products in the market, certainly improved safety. So what we want to ensure is that we'll have improved patient compliance, if you will. So entering the market with a subQ formulation of PMN310 is certainly in our sights. And we've actually started the formulation development of that program.
We've actually hired somebody on board to really lead the effort on the subQ formulation. We haven't presented any data or results on that. We will give some clarity as we get going with this program. We think it's quite possible—again, others have gone before us and formulated antibodies as a subQ formulation. So I don't think it's overly complicated, but understanding what's required—viscosity, volume—we need to understand the PK/PD and dose from the clinical study.
But all of that seems very, very possible. Again, without giving too much away until we do the actual data and the work, it does seem like it is possible. Then we need to understand how to roll it into that next study such that we can get it to become commercially available as soon as possible. But it is very much a priority for us, developing this over the next couple of years.
Pete Stavropoulos, Analyst at Cantor Fitzgerald
All right, great. And last question: you did touch on it—you do have early-stage candidates. Just curious to hear how you're thinking about these assets and which may enter the clinic next, and what's going to be the driving factor for those decisions?
Neil
Yeah, I mean, the driving factor is certainly going to be data and resources. And thanks for the question. We really are excited about the pipeline as well, although we obviously remain, as they say, laser-focused on the execution of this study to deliver the results on time and safely as well. But beyond that, there are some very exciting products coming along. I think our EPISelect platform is unique and differentiated in that we can—I think we've proven we can—develop very selective antibodies to these misfolded proteins.
So, as we said, coming close behind is the antibody targeting misfolded forms of TDP-43, which is implicated in most ALS patients—so ALS is another candidate indication we're going after. And then the misfolded forms of alpha-synuclein, whether it be dementia with Lewy body or Parkinson's disease, are also very interesting to us. So we are actually advancing both those candidates preclinically. We would like to get additional preclinical proof of concept for those candidates as well.
It would be important if we can generate data with the Alzheimer's program—clinical data—but then also have some preclinical proof-of-concept data in the follow-on assets that all read out in the same time frame. We want to demonstrate that we have a robust discovery engine, if you will, and a viable pipeline beyond Alzheimer's. So the goal is to advance the two pipeline candidates toward the clinic over the next six to nine months such that they'll be ready for IND-enabling studies and can enter the clinic within the next year or so.
That's very much a goal of ours, to advance these. Again, we're selective. The driving factor will be data, obviously, as it always is, and resources. Again, the bulk of our resources is focused on the Alzheimer's program, so we're careful how we allocate resources beyond that. So we're modestly allocating certain resources to advance a couple of the pipeline candidates as well in order to generate value and get those to the clinic for patients as soon as we can.
Pete Stavropoulos, Analyst at Cantor Fitzgerald
All right, great. Thank you, Neil and Larry, for taking our questions, and have a good evening.
Neil
No, thanks so much, Pete, really appreciate it.
Larry Altstiel, Chief Medical Officer
No, thank you. Thanks, Pete.
OPERATOR
Next question. Fazia Ahmed with Brookline Capital Markets, please proceed.
Fazia Ahmed, Analyst at Brookline Capital Markets
Hi, team. Thank you for taking my question. My first question is, I see on the press release you'll be presenting at the upcoming CTAD meeting. If you could share what you would be presenting at that meeting, that'd be great. Then I'd have a follow-up.
Neil
Sure. I mean, CTAD, for those of you who don't know—Clinical Trials on Alzheimer's Disease—is a medical conference focused on Alzheimer's, and that takes place in mid-November, and it's really kind of the next one. As you all know, we attended AAIC in July, and this is the next one following AAIC, coming up in November. We're submitting abstracts similar to what we presented already, Fazia, so we don't have any acceptance yet of abstracts, so we're careful what we're saying we're going to do at CTAD.
I mean, we are at CTAD; we're going as a team. It's in Boston this year, where we're located. But we plan on being at CTAD certainly to engage with KOLs, to engage with pharma companies, and with interested parties. Ideally, we'd like to present similar data that we presented a couple of weeks ago around the interim analysis. Again, we're not looking to present additional data, but if we're given the platform by the organizing committee at CTAD, it would be nice to stand on the podium and present again.
Again, we haven't been given that yet; they haven't decided on all the speakers. But we'll be there in force to talk to folks and, ideally, to re-present, if you will, the interim analysis that we presented a couple of weeks ago.
Fazia Ahmed, Analyst at Brookline Capital Markets
Thank you. And my next follow-up question is on the subQ formulation. So I just wanted to see if you could shed a little more color on, assuming the Phase 1b study is positive, how do you incorporate subQ? Would it be part of the potentially registration study, or would you expect to establish efficacy with the IV formulation first and then bridge to subQ separately?
Neil
Yeah, we haven't. I mean, those are things we're kind of asking ourselves internally. As I said, we're kind of building out that plan now. You know, the important thing is we get it to patients as quickly and safely as we can. You know, a lot depends on, you know, assuming the data is positive. A lot depends on clinical trial design. You know, that in part depends on FDA feedback. So there's a lot of moving parts. Fazia, on, you know, is it, is it a separate arm of a registration study?
Is it, does it follow? Does it come before? So we really haven't given any guidance yet on that. Again, a lot of these questions we're asking ourselves internally and with our experts. So as soon as we have some clarity around how the sub Q folds into the next clinical development piece, we'll certainly update the folks. But right now, as I said, there's a lot of questions that we need to answer first around dosing and viscosity and some of the stuff we're advancing now just to understand a little bit more.
Again, viscosity is an easy one to mention because that's something that needs to be done early. So these are the studies we're doing in order to understand, you know, we're also looking at, you know, kind of devices and is this an auto inject pen, for example? Does that make sense? So, again, a lot of questions to answer first before we know exactly, you know, how it plays out in the clinical development picture. But it is our intention to, you know, have a subcutaneous, instantaneous form of the product to patients, you know, as quickly as we can.
Fazia Ahmed, Analyst at Brookline Capital Markets
Thank you.
Neil
Sorry I can't be more specific. Again, there's a lot. There's a lot here, but we'll clarify. And it's not, it's not trying to be. To avoid the question. It's just, you know, as I said, we're determining a lot of this ourselves with our experts.
Fazia Ahmed, Analyst at Brookline Capital Markets
No, I understand. Thank you so much.
Neil
Thanks, Fazia.
OPERATOR
Next question. K. Nakae with Chardan, please. Go ahead.
Keay Nakae, Analyst at Chardan
Hi. Hey, Neil. Thinking forward to 2027 and assuming the Phase 1b data reads out positively, as you're thinking about the design for the registrational study, what can you learn that can inform the design of that study from the phase 3 studies of lecanemab or donanemab, whether it's, you know, patient inclusion exclusion criteria or your choice of the primary endpoint, you know, whether that's CDR-SB or iADRS, you know, what are you thinking there?
And how might those studies be helpful in your design? And maybe, Larry, I mean, I'll follow, but Larry, sure. You might have some thoughts around that.
Larry Altstiel, Chief Medical Officer
Yeah, I think the outcomes. The outcomes will be pretty clear. It's the. The FDA really recommends the CDR sum of boxes as the primary clinical outcome measure because it includes both functional and cognitive assessments. And then with the ADAS-Cog and ADAS-Cog composite scores, like the iADRS, you know, as secondary outcomes. So I think that we're pretty well fixed on what the outcomes will look like. In terms of what the trial design will look like.
You know, we think that obviously the trial will have to be, you know, of a large enough. Large enough size in terms of patients and a long enough duration to, you know, make some credible statements about, you know, affecting disease progression. And it has to be large enough that we can power it to see a credible change in the CDR sum of boxes, which will be the primary outcome. And it's important to note that, again, the primary things that are involved in getting an approval are, one, safety and then two, a positive clinical outcome.
So I think that we can learn something from their studies and something from their recruitment strategies and something about, you know, the time that it takes to enroll such a study. So I think that again, what we'll learn probably most of all is, you know, what's our effective dose from our Phase 1b study? What kind of clinical signal do we see in our Phase 1b which will help us power that larger Phase 3 study?
Neil
Yeah, we'll kind of give a little bit more color around that, K., too, as we decided. Again, those trials, those trials are certainly, you know, formative and give us some color as to, you know, a little bit of precedence. They were done a number of years ago. And also keep in mind that, you know, we certainly expect to go to the agency, the FDA with a much differentiated product, certainly with respect to safety profile. So when you look at the numbers of patients that the donanemabs and the lecanemabs Lilly and Eisai had to build for their safety database, we're expecting, you know, ours does not have to be that large if all continues well.
And as we've seen, so, you know, patient numbers might be less, again, powered for efficacy. Not because. Not because we need a large safety database. Again, we're not expecting a black box warning. You know, ideally our ARIA and safety profile, you know, would prevent that from happening. So there's certain things we can certainly learn. But I think, you know, I think our product's going to be differentiated in a very positive way such that there'll be, you know, there'll be elements of our clinical trial that make it, you know, more streamlined and such.
You know, we do expect to run a global clinical study. We want to make this product available to patients around the world. That's our kind of one of our, you know, philosophy here at the company. But also, you know, market size globally is interesting for us as well. So we'll get more clarity around, you know, the trial design as we interact with the agency. And again, we have fast track, so we can do that in a pretty expedited. In a pretty expedited way.
But I think it's going to be a, you know, differentiated enough product that we might be a little bit more streamlined in our approach.
Keay Nakae, Analyst at Chardan
Well, great. Great to hear. We'll look forward to hearing more about that.
Neil
Thanks so much, K. Really appreciate it. Operator, do we have one more?
OPERATOR
Yeah. Next question. Rajaram Selva Raju with HC Wainwright, please. Go ahead.
Yanzi, Analyst at H.C. Wainwright
This is Yanzi sitting in for Rom. I have two questions. The first is, so at top line, what magnitude of pTau217 or MTBR Tau243 change could you consider beyond assay and within-patient variability, and how will that placebo separation and dose exposure response factor into your interpretation?
Larry Altstiel, Chief Medical Officer
Yeah, I mean, go ahead, Neil.
Neil
Well, I'll just start quickly and then you probably speak to this better than me, Larry. I mean, again, as far as kind of expectations and what do we expect, we're kind of really being careful not to go into, you know, into the next six months and top line, you know, predicting what might happen. Again, we're, you know, we're expecting and we're hoping to kind of continue along the same framework here with clean safety, you know, and a strong clinical signal. So predicting what, you know, what expectation is tough at this stage. We want to be careful not to kind of give any guidance on these are the numbers or this is the level of separation.
I think we want to be at least as good as from an efficacy perspective, what's on the market when you look at, you know, expectations and biomarker movements and percent biomarker movements. Again, we don't want to give any expectations here. I know, Larry, maybe you can speak to the, you know, holistic approach of the biomarkers and I think we're very expansive with the panel of biomarkers that we're looking at. So that's kind of more important for us to think through mechanistic statistically how the drug might affect some of these biomarkers rather than kind of leading with, you know, we expect to see this percent change. But Larry, you can maybe speak to that a little bit.
Larry Altstiel, Chief Medical Officer
Yeah, I think, Neil, that's correct. We look at the biomarkers in their totality. We chose them, you know, really to reflect a lot of the biology that is affected by Aβ oligomers. We expect them, you know, to move at different times and at different magnitudes. But we think that they will tell the total story of what PMN310 is doing and I think it probably doesn't make a lot of sense is to tie, you know, success or failure to a particular percentage of pTau217, especially at this stage in the study.
So again, we look at the biomarkers in their totality and again, that will give us a more fulsome notion of, of the biology of PMN310 and also really help guide us and, you know, in our subsequent studies as well.
Yanzi, Analyst at H.C. Wainwright
Got it, thank you. And my next question is actually, you know, speaking of biomarkers. So with Svita, what controls, I'm curious, have you run to rule out PMN310 interference with assay capture or detection, you know, just for example, so that a lower signal reflects lower.
Larry Altstiel, Chief Medical Officer
Yeah. The answer to that is yes. Again with our new assay that we have that's being optimized right now. So I think we're in pretty good shape with that assay.
Yanzi, Analyst at H.C. Wainwright
Thank you.
Neil
Okay. Thank you. Thanks.
OPERATOR
I would turn the floor over to Neil for closing remarks. Yeah.
Neil
Again, I'd like to thank everybody for, you know, your attention this afternoon. It's been again, an interesting call. Thank you all. So to the folks for their very interesting questions. Appreciate that. And thanks for your attention, your interest in ProMIS Neurosciences and our programs. We look forward to presenting more updates over the remainder of this. Really an exciting and pivotal year for us at ProMIS Neurosciences. So thanks again for your attention and we'll continue to update you as we progress.
Thank you.
OPERATOR
This concludes today's teleconference. You may disconnect your lines at this time, please. And we thank you for your participation.
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