Hemab Therapeutics Holdings, Inc. (COAG) Q3 2026 Earnings Call Transcript

Welcome to the call. EMAB Therapeutics' third quarter 2026 conference call. Leading the call from Management are Benny Sorensen, Chief Executive Officer, and Mads Berndt, Chief Financial Officer. After Management's prepared remarks, we will open the call to your questions. To ask a question during the session, you'll need to press star 1-1 on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star 1-1 again. Please be advised that today's conference is being recorded. Before we get started, I would like to remind everyone that some of the comments that management may make on this call about the company's future expectations, plans, and prospects constitute forward-looking statements for purposes of the safe harbor provisions under the Private Security Litigation Reform Act of 1995. Actual results and events could differ materially from those expressed or implied in any forward-looking statements as a result of various important risks, uncertainties, and other factors, including those set forth in EMAP's most recent filings with the SEC, including its quarterly report on Form 10-Q, where the quarterly period ended September 30, 2026, and any other future filings that the company may make with the SEC. Any forward-looking statement represents our view only as of today and should not be relied upon as representing our view as of any subsequent date. You are cautioned not to place any undue reliance on these forward-looking statements, and HEMAB disclaims any obligation to update such statements except as required by law. A replay of this call will be available on the Investor section of the HEMAB website approximately two hours after the conclusion of the call. I will now hand the call over to Benny Sorensen, Chief Executive Officer.

Thank you, Operator, and thank you all for joining EMAP's first quarterly financial results call. We're glad you're here, and we look forward to using this forum every quarter to share our progress. At HEMAP, we are developing targeted therapies that reimagine the treatment of blood coagulation disorders to sustain life and human resilience. Our philosophy is simple, all patients matter, and people living with serious blood coagulation conditions should not have to live with inadequate treatment options. Let me start with the three pieces of news that matter the most for the coming months. First, yesterday, we announced the initiation of our pivotal phase-free trial of psotasamec enhancements from Bissenia. Second, last week, we also announced the first clinical data from our Phase IIb trial of Pseudasmec in Factor VII deficiency and new menstrual bleed data in non-human primates treated with HMB003. Updated data from the Factor VII deficiency trial will be presented at the ASH annual meeting on December 14th and the HMB003 data on December 13th. And third... In February, 2027, at the 20th EAHAT Congress, we will present new data from our HMB002 program in von Robben's disease. These updates follow a remarkable stretch for HEMAP. Since our IPO in May, we have not slowed down. In July, we put our science on the global states at ISGH with nine presentations and data updates across all three of our programs. We unveiled HMB-003 and dosed the first participant in our Phase I trial. And we've now initiated SOLARA, our pivotal Phase III trial of Cytasomec in Glantzman's Frombasthenia. It's our first pivotal trial, and it's the first pivotal trial of a subcutaneous prophylactic treatment in Glantzman's Frombasthenia. Truly a defining moment for HEMAP and for the Glantzman community. As we move into late-stage development, we are building the organization to match our ambition. In September, we welcome Kelly Wahlberg to our board. Kelly brings two decades of commercial leadership, including launches of medicines for conditions ranging from rare to very common, making her the perfect strategic match. We have also begun building our commercial strategy and team so we can position ourselves to bring our medicines to patients as quickly as possible. Across our programs, we listen to patients' lived experience, we quantify the neglected unmet need, we apply our deep coagulation expertise, and we use validated technologies as well as high-quality clinical development strategies. We believe a different future is possible, one where prevention, not just management, becomes the standard of care. That vision comes to life across our first three programs. Tassamec is being developed for both Glantzman's Pharma's Genia and Factor VII deficiency, with approximately 10,000 patients in our key markets. HMBO2 targets from Robbins disease, the most common inherited bleeding disorder with approximately 120,000 diagnosed patients in the same key markets. And HMBO3 targets heavy menstrual bleeding, which affects more than 23 million women in the United States alone. I'll walk through each program, MASC will review the financials, and then we will take your questions. HMB003 is a fatty acid conjugated peptide that inhibits plasmid directly at its active site to stabilize clots. Preclinically, it showed greater activity than tranexamic acid, today's primary non-hormonal therapy for heavy menstrual bleeding, and PK properties supporting potential once per cycle dosing, potentially offering an improvement over current short-acting therapies. We are initially developing HMB003 for heavy menstrual bleeding, which has been called the missed vital sign and is too often ignored. It is reported in roughly one in three women of reproductive age and is the leading cause of iron deficiency and anemia in this population. According to data compiled by Wellcome Leap, affected adult women miss an average of 3.6 weeks of work annually, costing the U.S. economy an estimated almost $100 billion. Millions of women and girls have no approved non-hormonal customized hemostatic treatment option for heavy menstrual bleeding, and that is the gap we are working to close with HNB-003. In September, we dose the first participant in our randomized, placebo-controlled, single-ascending-dose Phase I trial in Healthy Volunteers, which will inform dose selection and clinical development plans for HNB003 in heavy menstrual bleeding and across additional high unmet knee bleeding conditions. We expect initial clinical data from the Phase I trial in mid-2027. We have also announced new preclinical data from a synomalcus monkey model of menstrual bleeding in which HMB-003 reduced the proportion of severe bleeding days and shifted bleeding towards lower intensity compared with baseline. We'll present these data at ASH on December 13th. HMB002 is a subcutaneous prophylactic monovailant antibody designed to shield veneropin factor from degradation, raising the body's own levels of both veneropin factor and factor VIII without compromising function. At ISGH, data from the Valora Pioneer Phase 1-2 trial showed clear proof of mechanism, and candidly, the results exceeded our own expectations. We had set a 1.5-fold increase as the target product profile, but we saw peak increases of approximately 2.5-fold in both Envelopment Factor and Factor VIII, with normalized rombin generation and APTT, and durability supporting potentially monthly dosing. Most adverse events were mild to moderate, with no series of dramatic events. The single ascending dose portion was not designed to measure efficacy, so the early clinical observations were descriptive in nature. Still, We find them encouraging. Based on prospectively collected data, eight out of nine evaluable patients had zero treated bleeds in the 28 days after dosing, with a mean annualized treated bleed rate of 1.6 compared with a baseline mean of 20.1 prior to treatment. The law of DISCOVER continues its successful enrollment with now 110 patients in prospective run-in and identified for future interventional trials. At EAHAD in February, we expect to present initial data from Part B, monthly subcutaneous dosing at 150 mg, and additional Part A data from single dosing at 300 mg. These data will cover patients with both type 1 and type 2a disease, adding data from 8 to 10 new patients with a total above 20 patients already. Lastly, let me turn to Cytasomec, a bispecific antibody that binds and stabilizes the body's own factor 7a and recruits it to activated platelets to facilitate the formation of hemostatic plucks and control bleeding. In Glouncement Thrombusthenia, it holds FastTrack, OffAndRock, and Breakthrough Therapy designations from the FDA, along with regulatory designations in Europe and the UK. Starting with factor VII deficiency, a severe bleeding disorder affecting about 1 in 500,000 people, where bleeds are recurrent, unpredictable, and potentially life-threatening. A FACE-II-B trial is ongoing at a single site in the UK. At ISGH, preclinical data showed binding to 22 of 25 tested severe to moderate factor VII variants, or 88%, supporting a broad patient applicability. Last week, we announced our first clinical data from the single ascending dose cohort. As of July 24th, two participants with severe congenital factor VII deficiency had received a single subcutaneous dose. Adverse events were low-grade and assessed as not related to treatment. Baseline pro-frombin time of 180 seconds or more, shortened by more than 50% in both participants. In the participants with PK and PD data available, Pseutazomic produced sustained multifold accumulation of endogenous total factor VII, with exposure maintained through day 22. Updated data from all those participants will be presented at ASH on December 14th. And now, glancements from Bestinia. And here is the part that matters the most. There is no approved prophylactic treatment, and care today is reactive rather than preventive. The burden is felt week after week. In Glansman's 360 and International Natural History study, 88% of participants reported at least one bleed in the previous week, and 65% required a bleed-related hospital visit in the prior six months. These patients, or these people, they have kind of normalized living with unpredictable bleeds. Against that backdrop, our Phase II extension data from ISGH gives us real conviction in this program. They showed sustained bleed reduction in 34 participants at a median of 6.9 months and up to 15.9 months of exposure. 92% of participants who bled during the run-in had fewer treated bleeds on Sotasmac. The mean high-intensity annualized treated bleed rate was reduced by 62%, and in the low-dose weekly cohort, the mean annualized treated bleed rate fell by approximately 80%. There were no Grade 3 or higher related adverse events. Three participants had Grade 2 thromboembolic events in higher exposure cohorts and or with multiple risk factors, all managed with routine anticoagulation therapy. Based on these data, we have now initiated Solara, an open-label, single-arm, multicenter trial enrolling approximately 75 people with glansman's thrombusthenia aged 12 to 70, with at least four treated leads in the prior 12 months. After a 24-week run-in on current treatment, participants received 48 weeks of once-weekly subcutaneous cytosimic at 0.2 mg per kg, a regimen chosen with the goal to optimize bleed reduction while avoiding the high peak exposures associated with the observed thromboembolic events. The primary endpoint compares the annualized treated bleed rate on Cytasomec with the run-in period, with each participant serving as their own control. Secondary endpoints include high-intensity bleed rate, safety tolerability, immunogenicity, and pharmacokinetics, and participants who complete treatment will have the opportunity to continue Cytasomec in a separate open label extension study. Solara is being conducted under HEMAP's active IND. Solara is designed as a single arm trial using intrapatient comparisons. The FDA recommended that we consider a randomized controlled trial. However, the FDA acknowledged our concern about the feasibility of randomization in announcements from misthenia. In light of substantial variability in treated bleed rates, the heterogeneity of the patient population, and the practical consideration of randomized trials and rare diseases, we've determined to proceed with the single arm trial. Solara is a landmark for the Glansman Pharmacenia community. The first participants have been consented and are scheduled to enter the run-in before end of the year. With that, I'll hand it over to Matt.

Thanks, Benny. I'll do a brief financial review. Cash, cash equivalents, and marketable securities were $430.2 million as of September 30, compared with $457.5 million as of June 30. We continue to expect our cash to fund operations into 2029. R&D expenses were $24.6 million for the third quarter of 26, compared with $14.6 million for the third quarter of 25. The increase was primarily driven by advancements of our clinical programs and higher personnel costs. G&A expenses were $5.1 million for the third quarter of 26, compared with $2.5 million for the same period last year. Net losses for the third quarter was $27.3 million, or $0.58 per share, compared with $17.1 million, or $18.04 per share for the same period last year. With that, I'll now hand over the call to the operator to open the line for questions.

As a reminder, if you'd like to ask a question at this time, please press star 11 on your telephone and wait for your name to be announced. To withdraw your question, please press star 1-1 again. Our first question comes from David Nierengarten with Wedbush Securities.

Thanks for taking the question. I had a couple. Just on the first one with the FDA feedback on the sutessomite study in Glantzman, did they give any other rationale for their desire to have a randomized controlled trial besides it being a gold standard, so to speak? It seems to be hard to match patients in this population, and then the second one was, as you reported out before in previous data, The VTEs, one patient had VTEs, was obese in that study in Glantzmann, and I was just wondering if you had a weight range for inclusion into the study. Thank you.

Thank you, David, for the question. Hey, let me elaborate a little on the Solara and the regulatory path there. As I just mentioned, Solara is designed as a single-arm trial using an intrapatient comparison, which is a common registrational path in bleeding disorders. And in particular, Positasamec in glansman's thrombostinia. We are really following the observed clinical data from the 34 patients in our phase two. As you may recall, in a bleeding disorder like Glantzman that really has been honestly deprived from any innovation for decades, unfortunately, the treatment guidance, the practices, they vary very significantly, and a single-arm trial is really the strongest way to control for that variability. You guys also know that we have a breakthrough therapy designation, fast track, often drug, and we do enjoy really close dialogues with the agency on how best to advance sotasomec and glansman thrombusthenia. So with the extensive amount of dialogue we've had, we have implemented lots of the constructive feedback. Yes, the FDA recommended that we consider a randomized controlled trial. However, at the same time, acknowledge, you know, the variability that we are seeing and the concern about feasibility of randomization. And, you know, in particular, giving the substantial variability in treated bleed rates, the heterogeneity in the patient population, and some of the practical considerations for a randomized trial, we believe this is what the data is telling us is the right thing to do going forward. And just lastly, as you all know, plenty of precedents for single arm trials in bleeding disorders. Just to mention a few, in von Robben's disease, both Von Bandi and Will 8 did single arm hipopsy in hemophilia A and B. It happened, which is a factor 13 concentrate and factor 13 deficiency also all ran, you know, prophy registrational trials as single arm studies. So we have a high degree of confidence. This is the right path forward. To your second question, David, on weight ranges, I forgot what the top weight range is in the eligibility criteria, but hey, here's the good news. The study will shortly be available on clinicaltrials.gov, and I'm sure that that specific eligibility is probably in there, David. I'll have to follow up with that.

Okay, thank you.

Our next question comes from Corey Kazimov with Evercore ISI.

Hey, Benny and Matt. This is Josh on for Corey. Thanks for taking our question. Ours is on Von Willebrand. Probably the most common investor question we get is what we should be expecting as far as amount of follow-up and any of the efficacy markers or PKPD data that we should be focusing on into that data. Thank you so much. Thank you, Josh.

Yeah, let me elaborate on that, too. Excited to kind of give an update on the HMVOO2 data at IAHAT in February. And just kind of like go through it step by step. There'll be additional single ascending dose data at 300 milligrams. We are hoping to see a maximum accumulation plateau around two to threefold. And I think that the 300 milligram will be particularly informative for that. And if we then look at the PK that we already have on 20 milligrams, 50 milligrams, and 150 milligrams, we might also see that the 300 milligrams is a dose that could last a little longer. But hey, let's see the data, what it tells us. On the multiple ascending dose, it will be 150 milligrams. Similarly, here, we are hoping to see an average of two to threefold accumulation of enveloping factor and a support for the once monthly dosing. With regards to the clinical activity, we have said all along, right, we want to see more than 50% reduction in the annualized treated bleed rate. Yes, more is better, and it's still somewhat early days. And I think the last thing to emphasize... We will also be presenting data from both patients with type 1 and type 2A, and when you look into the population, that is really covering the vast majority of patients with enrolment disease. Thank you.

Our next question comes from Rich Law with Goldman Sachs.

Hey, guys. Good morning. So I'm actually kind of surprised that the FDA asked for the randomized control trial since we saw many pivotal trials in Hime and VWD using single-arm trials that you pointed out. I mean, at this point, do you have full alignment with the FDA, or do you believe you're taking some risk with a single-arm trial? And also, like, how did you and the FDA end that discussion? And then I have a follow-up.

Yeah, I think, as I just alluded to, Rich, I think, by the way, we have a high degree of confidence this is the right trial, in particular, taking into account the patient population, the empirical data we generated in phase two, giving us deep insight to the variability of leads. And, you know, our regulatory friends here, they really acknowledge that, right? I think when they're saying, you know, recommend, consider, that is probably for good order. And I think it's equally important that they acknowledge, you know, the concern in running, you know, a conventional randomized controlled trial, in particularly in a bleeding disorder that has never, ever had a prophylactic drug developed. So I think the risk is very low here. And, you know, good news is we will continue dialogues with regulatory agencies, including the FDA going forward. The more we talk, the more we align. So I'm very confident that this is the right path forward, Rich. And you had a second question, right?

Yes. Yeah, the second question is that at the ASH, I think we saw the ASH abstract you showed. I think there were two patients for that Sector 7 deficiency. Just want to see, like, is there any more that we're going to see? What's the endpoint? What's the final sample size that we should see at the ASH presentation? Thank you.

Yeah, I think, you know, let me also go into that. I'm very excited about sharing our Factor 7 data at ASH. And we're really aimed here to generate what I call like a binary data readout in a very small number of patients, pretty much trying to recapitulate the non-human primate study in patients with Factor 7 deficiency. And at the same time, validate all of the molecular biology studies that we have done. We further aim to kind of show that our entire preclinical package with the preclinical NHP, the molecular insight into mutations, leading to factor VII deficiency. And that knowledge of what mutations generate factor 7 variants that can bind to TASMEC and what mutations are less likely to bind, pretty much hoping to see that the molecular diagnosis can be an immediate predictor of when you have a responder or whether you have a non-responder. We're not elaborating on the number of patients, but I think I've been clear here that it's a very small number of patients, a study conducted just at one site in the United Kingdom. But I truly believe that this data is going to be sufficient for us, by the way, to make a substantial additional investment in Factor 7 deficiency going forward.

Great, thank you.

Our next question comes from Maury Raycroft with Jefferies.

Hi, good morning. Thanks for taking my questions. I was going to ask one on Glansman as well for the Phase 3. Just wondering if there were just minimum ATBR reduction thresholds, run-in bleed rates for interpatient control, or any statistical aspects discussed with FDA that you could talk more about today, and what bars for success would be that would give you confidence around the potential regulatory risk?

Yeah, I think, by the way, very shortly, Mori, the entire eligibility criteria will be available on clinicaltrial.gov. We have like a minimum annualized treated bleed rate of four going in to make sure we, you know, we can't completely eliminate a zero, but this should substantially reduce any patient coming in with zero.

Got it. Okay. And, uh... And maybe a follow-up on just with ASH coming up, we're expecting longer-term Insight Star Open Label Extension data there. There's likely going to be compare and contrast with your OO2 EHAD data. So I'm wondering if you think we'll get perspective into differentiation at EHAD on bleed control, maybe safety profile, or stronger activity across different subtypes for vulnerable brands.

Yeah, you know, as I said, we will be presenting data on type 1 and type 2As. As you also know, it is really, really hard for us to do a direct comparison between HMBOO2 and other ongoing programs as we have taken kind of distinctly different kind of approaches in the way that we are collecting the data. I think, in particular, we count bleeds that need treatment, and we are collecting those prospectively. We know that this is an endpoint that is used in registrational trial and bleeding disorders, so we're giving us a high degree of confidence. And I think it's just very important for us to emphasize a treated bleed is one that is serious enough that the patient needed medical intervention to stop it. Importantly, we collect this prospectively using a validated electronic bleed diary. We have at least four months of baseline run-in, and what you will see at EAHAT is up to four months follow-up afterwards on treatment with HMP002. And I think the other thing I want to emphasize is right now, enrolling both type 1, type 2A, our Valora Discover study with more than 100 patients worth of kind of natural, prospectively collected natural history data is really a goldmine for HEMAP right now and giving us an increasing amount of confidence on being really data-driven and smart. It's in our next steps of development.

Got it. Thanks for the perspective.

Our next question comes from Joyce Cho with J.P. Morgan.

Hey, guys. Thanks for taking our question this morning. For Solara, can you provide any additional color on discussions with the agency around safeguards with respect to cardiovascular risk screening, anything that came up in your discussions that was new relative to your expectations, or was everything, you know, fairly in line? Thanks.

Yeah, Joyce, I am super proud of the way we have approached this. We have got a lot of praise from the regulatory authorities here in the way that we have designed our safety monitoring plan, the way that we have developed the eligibility criteria to be for all patients with glansman thrombocemia, but of course, safeguarding the molecule with the knowledge that we have. So I would say absolutely no surprises with regards to the way we have designed legibility and safety monitoring, and I'm super proud of that because that means we have done the right thing from a clinical development point of view.

Our next question comes from Gaurav Maini with LifeSci Capital.

Hey, good morning, everyone. Appreciate the update this morning. So one thing that, you know, KOL has noted to us and that they really appreciated from our combos is that you can actually measure Von Willebrand factor given the mechanism of HMB-002. And in some points they note here, right, titrating, inadequate responders, confirming patients aren't pushed to, say, several hundred percent, et cetera. I guess with this, how do you think about potential differentiation here, especially as we think about other late-stage competitors out there? And then I do have a quick follow-up.

Thank you for that point and that question. I think this is probably the ultimate strength of HMBO2. It is simple, it's intuitive, it directly targets, it directly corrects the underlying pathophysiology, and it is readily available for the clinicians to monitor whether the treatment is having the intended pharmacological effect. So, I think that that is a key differentiator. And remember, we are pretty much standing on the shoulders of 50 years of clinical experience with regards to this as a mechanism, because this is exactly what you can do with DDAVP. You can give DDAVP. You can monitor the relevant factor. You can monitor factor 8. We know that that's a very effective way of controlling an acute bleed management, but of course, you know, not possible at all to use as a prophylactic therapy. But mechanistically, this is right in the wheelhouse of practicing hematologists and bleeding disorders. So I think that's a huge differentiator. We can simply just measure what they've always measured, monobulman factor and factor VIII. I'm excited about the data we presented at ISGH. I'm just reflecting a bit more on those. Give or take 2.5-fold increase in monrobin factor and factor 8. The population we are stuttering, on average, have about 20% monrobin factor and about 35% factor 8. So you do that 2.5 times that, you get on average into the normal range of aerobin factor and factor 8. That would be, for a treating clinician, I think that could be very reassuring for a lot of patients. So I think you are spot on. I think that is a very clearly differentiating.

Yeah, and appreciate the color there, Benny. A quick follow-up. So, for von Willebrand disease as well, you know, this kind of bar that the company's been guiding to have ATBR of at least 50% reduction. Can you just remind us where that number comes from?

Yeah, that comes from the last, I guess, 45 years of development of drugs for bleeding disorders. It has been a clinically meaningful criteria. It's been a regulatory criteria. More than a 50% reduction in treated bleeds is considered clinically meaningful. And then, hey, more is better. There's no doubt about that. But while this is still a young, you know, ongoing phase one, two trial, I think we'll keep it there. If the data looks much more favorable, we can always dial up the expectations for that. But I think for now, that's the right guidance to give.

Awesome. Thank you.

Our next question comes from Michael King with Brodman and Renshaw.

Good morning, guys. Thanks for taking the question, and congrats on your progress. I hate to drag you back. to the regulatory discussions, but I just had a couple of follow-up questions about it. Was there any, Benny, was there any consideration given to alternative randomized trials, such as either two-to-one, three-to-one randomization, or, you know, brief periods where patients We would be treated with tranexamic acid and then, you know, then proceed on to Cetacimig or any other types of protocols that might have, you know, been compromised with the agency.

Yeah, I think, Michael, thank you for that. Thank you for that question. I can say it like this. We have turned every single possible stone to kind of make sure that we design the best possible trial with the highest probability of technical success here. So, yeah, I think we have elaborated on all possible trial designs. The reality is, as I keep coming back to, that with the empirical data we have, we can acknowledge very substantial variability in the bleeding patterns and in the treatment patterns. And, you know, one can then say, oh, couldn't you just dial down that variability, assume that it will be better in the future, and then you could have designed all sorts of other designs. But Michael, here's the reality. When you do a phase two trial in about 15, 16 sites, you get that variability. When we dial it up to a pivotal trial with approximately 75 patients enrolled across multiple countries, multiple sites, you know, that variability is rarely going down. It is more likely to stay the same. So, after a lot of iteration in that data and a lot of dialogue with our regulatory friends, this is the right study design to carry forward to give patients and us the highest probability of a drug going all the way. Okay.

And then, was there any consideration given to geographic split of the trials? I know this is something that affects consanguineous populations, so was there any minimums, maximums, or expectation of distribution of different geographies to make sure that there's at least some variability in the populations?

Yeah, you know, by the way, we have really only selected, you know, countries and sites that fulfilled the extensive visibility that we have conducted. So, you know, there will be, you know, a reflection of the variability of the population across, you know, geographic regions around the world. But we have been pretty strict with regards to countries and sites, investigator qualifications to make sure that we somewhat control, you know, the study conduct process. So, yes, right now the study is open here. It's already approved in a couple of other regulatory jurisdictions. And we'll kind of keep on updating you as we progress with the trial on what that distribution will look like over time. Yeah, right now, you know, go on the Solara website and see our... Recruitment activities here in the United States. I'm super proud of the way we are prepared for this and the way we are conducting ourselves for this trial.

Okay, great. And then one quick one on Willebrand. Insight's got data at ASH in Phase 3 right now. How do you anticipate navigating around their presence in the clinical trial setting?

Yeah, thanks, Mike. That, you know... I think this is where I usually say innovation is good for patients. So, I am first and foremost cheerleading for HMP02. I believe we have the molecule with the more intuitive, simple mechanism of action. I think we have a molecule that you can monitor. I'm super excited about the data we have so far. I really don't pay much attention to where our competitors are, emphasizing instead, you know, the qualities and the strength of our molecule. And I think what we have heard from the clinical community is that there's a high degree of excitement for HMPO2. So that's the wave we are running.

I'm not worried about competition in this particular space here. Thanks for taking the questions, buddy.

That concludes today's question and answer session. I'd like to turn the call back to Benny Sorensen for closing remarks.

Thanks. Let me just end here and say I could just not be more excited about where HEMAP is today and where we are going. With Solara, HEMAP has now begun its transition to a late-stage clinical company. Over the coming year, we expect updates across all our programs, starting with ASH in December, EAHAT in February. And we believe we're well positioned to reset the standard of care across coagulation conditions of every size. At HEMAP, all patients matter. And we are driven to give people living with serious coagulation conditions better options than they have today. And we are just getting started. And thank you to the HEMAP team, our partners and collaborators, and most importantly, to all of the health volunteers and patients who participate making this work possible. Thank you all.

This concludes today's conference call. Thank you for participating. You may now disconnect.