Operator
Good day, and thank you for standing by. Welcome to today's discussion with BridgeBio, which will cover the company's accurate CM Phase III results as presented at ESC. Currently, all participants are in a listen-only mode. Please be advised that today's conference is being recorded. I would now like to introduce you to the speakers for today: Julian Gillmore, MD- Professor at University College London and Head of University College London Center for amyloidosis and asomyloidosis center research fleet; Jonathan Fox, MD-PhD Chief Medical Officer of BridgeBio Cardio Renal I will now hand the call over to Neil Kumar, PHD CEO of BridgeBio. Please go ahead.
Neil Kumar
Thank you, operator, and thanks, everyone, for joining. The team has assembled here in Amsterdam, where we had the privilege of sharing further details from our attribute-based II clinical trial results of apparatus and ATTR cardiomyopathy. I used the word privilege on multiple levels. Number one, that with these data, we have the opportunity, as we previously discussed, and the responsibility to serve patients as broadly as possible with this drug and two, that the data reported in the clinical science story that will continue to build are only possible with the tireless work of the physicians that participated in this trial.
I have the opportunity to meet many of our esteemed physician partners this week, and we are energized by the passion to help patients with this medicine. No one exemplifies that more than Dr. Julian Gillmore, who we have a good portion of having our call today to review the data in some detail, and who is playing an incredibly important role in the development of ours and other imported therapies in this space. Moving to the presentation now. I'll be calling out Slide # progress. And on Slide 3, you can see the structure of the discussion today. I will briefly motivate the discussion with a reminder of the molecular hypothesis that underpins [ Aravanis ] in its development. I'll then turn it over to Dr. Gilmore to speak more about the Phase III clinical data, and then I'll return briefly to contextualize that data and provide next steps for the organization.
Moving to Slide 4, a brief reminder of the design principles that motivate our best-in-class stabilizer hypothesis. The first and most important design principle is to maximize stabilization, therefore, minimizing the production of toxic monomer. At least 3 strains of evidence suggest to us that in doing so, we can optimally impact patient health. Firstly, the well-established genotypeotype of the disease in the context of the variant population shows us the variance associated with greater levels of tetramer destabilization, presenting a more complicated form that do less restabilizing variance.
Furthermore, the existence of 2 prominent [ transorapressir ] mutations highlights that every greater decrease of destabilization in the context of a pathogenic mutation are correlated with better outcomes for patients. The so called T119M rescue mutation is the most potent of these destablilizer and it's often the full rescue of the disease provided with blueprint of our own drug program. The second side of evidence adjusting that ever better stabilization improves clinical outcomes is the ATTRACT trial run to understand the impact of tafamidis in the ATTR the population. In that trial, the 80 mg dose of the drug, which is about a 50% stabilizer of detailed depositors, regulatory submissions, outperformed the 20-mg dose, which is approximately a 35% stabilizer.
The final strength of evidence comes from ATTR polyneuropathy studies where again, everglade stabilization or toxic monomer reduction via knockdown provided ever better benefits to patients. Understanding the dangers across crop comparisons, we nevertheless observed that Tafamidis 20mg was outperformed clinically by high-dose diflunisal, which achieves close to 70% stabilization. Furthermore, the diflunisal result [indiscernible] which is a 70% [indiscernible] knockdown agent, suggesting we have similar quantitative levels of knockdown and stabilization lead to similar outcomes.
Again, consistent with the biochemical models of the disease driven by TTR disassociation and toxic monomer production. Finally, participant with 84% new max knockdown seem to outperform the 70% stabilizer in knockdown agents. The second design principle is to preserve the native [indiscernible] TTR is highly evolutionarily conserved with no known species, including humans, being capital in sufficient or null for the protein. Further, the protein is maintained a high concentration being one of the most 20 most abundant protein in the sera and its relatively short turnover time suggest a higher get cost for keeping it around. We place known goals in bio transport to the eye. Moving to Slide 5, I'll briefly review the tenants of superior stabilization that was built into Acoramidis.
First, the drug sees more target owing to a much lower degree of value binding than [ ascetic] Second, the drug demonstrated superior binding to the target implying a smaller 2. And finally, the drug does a better job of gluing the target together upon binding, employing a native finding both and inducing hydrogen barking at the bottom of the thyroxine binding pocket to super stabilize detector. This action essentially feel of the aforementioned T119M dust mutation. Slide 6 is that we reviewed the call with you in the past, the in vitro and in vivo signatures of superior stabilization have been documented and published on. I will go through these details today in the data in detail to provide them for reference or questions later if there are any.
Now let's move to Slide 7, where we see new data here that were presented at this week's ESC meeting. On the y axis of the presented charge is the percent stabilization as measured in our Western blot assay and the x axis are listed common variants associated with TTR. Two points stand out from these data to me. Number one, that Acoramidis is able to stabilize consistently across the varying spectrum and that two, Acoramidis stabilization reliably outperforms Tafamidis at clinically relevant concentrations. Moving to Slide 8. We represent the data that we shared a few weeks ago, showing in a post-hoc exploratory analysis that took advantage of the fact that the faint was allowed for drop in our trial that we were able to measure the mean change from baseline of serum TTR, a good in vivo reflection of stabilization. On the chart, you can see here that Acoramidis outperforms Tafamidis in this same trial and consistent with biochemical studies, not further outperformance is observed from the combination of agents.
Consistent with studies showing that Acoramidis displace [indiscernible] relevant concentrations. Okay. With that as a backdrop, I'd like to turn it over to Dr. Gilmore to present the detailed Phase II data.
Unknown Attendee
Thank you, Neil. It's a great pleasure to present to you the results of the tribunal Acoramidis in transport [indiscernible] Next slide, please. So ATTRibute-CM was a randomized double-blind plasma controlled trials 30-month 6 treatment duration, a schematic of the overall study design. Heritability criteria shown on the left, eligible patients had a diagnosis of ATTR [indiscernible] established either on biopsy or not inflatively and [indiscernible] 32 patients were randomized 2:1 to Acoramidis or mention placebo. Use of open-nettable was permitted after 12 months, if locally available and the discretion of the investigator.
The 30-month primary endpoint was a hierarchical analysis using the Finkelstein-Schoenfeld method of all-course mortality frequency of [indiscernible] change from baseline and Ng [indiscernible] from baseline and 6 million wall distance. At the end of the 30-month plan intervention period of all eligible participants were invited into an open label long-term extension. Next slide. The study ones are well balanced at baseline in terms of patient demographics and disease characteristics. Min age is 77 and most participants were male, just under 10% with TTR variant carriers. Median NT [indiscernible] characteristic of this patient population, randomization was also stratified according to these characteristics, which are widely used in clinical practice to stage the disease.
As expected, mean serum TTR was at the lower end of the reference range. And as I mentioned earlier, compromises committed after 12 months and was considerably more prevalent in the placebo offer. Next slide. The study met its primary endpoint with a highly statistically significant p-value of less than [indiscernible] Importantly, 58% of the win ratio times in the primary high hierarchical analysis were [indiscernible] by the first 2 components of the primary animal cause mortality and cardiovascular postilion and an analysis using these 2 components of the primary endpoint alone was statistically significant in its own right.
The results were consistent across subgroups with the point estimates favoring our ground is of the placebo and confidence in fast variety of unity with a few exceptions. Next slide. Putting our attention to the components of the primary endpoint you see the capital market curve of cumulative all cause mortality. The treatment effect favorite Acoramidis or a placebo with an overall survival of 81% on Acoramidis of 30 months which represents an absolute risk reduction of 6.4% on a relative risk reduction of 25%.
Next slide is 78% of the debts were cardiovascular in nature again, the treatment effect favorite Acoramidis over placebo with respect to cardiovascular related portal, representing an absolute risk reduction of 6.4% on a revenue risk reduction of 30%. Acoramidis treatment was associated with a 50% reduction in cardiovascular hospitalizations that was in itself highly statistically significant with a p value of less than [indiscernible] Again, the results were consistent across subgroups with the point estimates consistently favoring Acoramidis over placebo and confidence [indiscernible] to the left of unity with a few exceptions.
Moving on. We see that Acoramidis treatments associated with the blunting of the progressive rise in NT-proBNP, which is characteristic of this patient population and has been shown to be a clear prognostic value uses. The results were highly statistically significant in 30 months. Similarly, the treatment effect with respect to effort tolerance as assessed by 6-minute war distance favored attend this, and this was also highly statistically significant and clinically meaningful resulting in a 40-meter difference at 3 months. Relative preservation of quality of life was evident when patients on Acoramidis from the beginning of the 30-month observation period, mirroring the early separation of NT-proBNP that you saw in the last slide. Difference of 30 months was highly statistically significant.
Consistent with the molecular mechanism of the drive of preclinical data demonstrating near complete stabilization of therapeutic drug concentrations. Serum TTR and an in vivo ever a reflection of increased stabilization was probably a persistently innovated throughout the trial. This data are consistent with previously reported data from Phase I and II trials in healthy volunteers and patients with ATTR or cutting of in respect. Among the patients who reached 30 months, a higher proportion of Acoramidis treatment experienced by a reduction in NT-proBNP or an increase in 6-minute walk distance from baseline to 30 months. Acoramidis cohort experienced a reduction from baseline in NT-proBNP and 40% of patients actually award further at 30 months than they did it based.
Taken together, these data indicate benefits across the board with Acoramidis and the tantalizing the possibility of genuine clinical improvements on the drug. And you see a high-level safety summary of the data overall Acoramidis generally well tolerated with no filings of potential clinical concern. The incidence of premium emerging adverse events was balanced between the arms and the favored Acoramidis with respect to treatment emergent serious adverse events. Next slide.
In conclusion, the results of the ATTRibute-CM trial are robustly positive. The study met its primary endpoint with a highly statistically significant in value of less than [indiscernible] and a consistently positive premium effect across all imposed proper endpoint and across patient [indiscernible]
Accordingly, 58% of the win ratio ties in the primary analysis were provided by the first 2 components of the primary endpoint, all-cause mortality and cardiovascular hospitalizations, and analysis was significant in its override. Remarkably 30-month survival and cardiovascular hospitalization rates among patients on Acoramidis approach those in an age match population without ATTR and [indiscernible] And the emerging safety profile by Acoramidis remains reassuring with no safety signals of potential clinical concern identified in the stock. Back to Neil.
Neil Kumar
Thank you, Julian, again, for your leadership and dedication to patients in this program. I'd like to wrap by addressing questions we've been receiving from the physician and investor community alike. How we understand these data in the context of past trial data and in the context of today's patient population. Obviously, there's been no double run a head-to-head trial reforms. So cross-trial observations must be taken with a strong caveat in mind, although I honestly you should run a double [indiscernible] the future.
On Slide 23, we remind everyone of the same outcomes that we believe are consistent with the molecular test class hypothesis at the beginning of today's call with simply, we find ATTR-CM patients surviving more and going to the hospital less than has ever previously been observed in clinical studies to our knowledge. This adds to levels of risk reduction and actual patient improvements that also have not been previously observed to our knowledge, and it reinforces the tie, I discussed between ever better levels of stabilization and ever better clinical outcomes.
Moving to Slide 24, we observed that the 30-month survival on Acoramidis in this trial is 81% remarkably close to Dr. Gilmore suggested in the 85% [ actuarialize ] expectation absent ATTR-cardiomyopathy for our clinical trial population. This suggests a dramatic reduction in ATTR cardiomyopathic death risk. Furthermore, we observed this observation with a near normalizing of hospital frequency, a key measure of morbidity in this population.
The absolute balances of survival and hospitalization are a little superior to what has been observed in prior trials. Moving to Slide 25. I'll remind everyone of the data Julian presented regarding improvement in NT-proBNP and 6-minute access and further highlight that these improvement characteristics are almost twofold higher than what has been observed in prior trials. Finally, on Slide 26, when connected dots between stabilization and clinical appliances using our internal trial data set. For the sake of time, also is only on Box four whereas for the first time, we look at correlations between key outcomes with continuous variables and sure TTR levels on drug. In an exploratory post hoc analysis of the relationship between the on-treatment [ seraTTR ] levels and on treatment measures of CDH, NT-proBNP and KCCQ there are buses association between the mean on treatment TTR level in each of these 3 variables.
This suggests that restoring serum TTR to mid-upper values of the reference range is associated with better outcomes at the subset level. All figures in Box 4 have a p-value of less than 0.0001 for the correlating test. The line in each plot represents the wear when you invest it. Okay. I'd like to wrap up and quickly with next steps on Slide 28, you can see that we anticipate -- we continue to anticipate on our NDA by the end of the year. And on Slide 29, I'll just remind you briefly that these data being presented today represent an exciting starting point, not a pending point for further data analysis and generation. In particular, we're quite excited for what needs to come at AHA. So please stay tuned for that.
And with that, I will turn the discussion back over to the operator for questions.
Operator
[Operator Instructions] Our first question comes from [ Celine Syed ] with Mizuho.
Unknown Analyst
Congrats on the additional data. A few for me, if I can. Number one, just on safety. I know there's been a lot of focus on efficacy over the course of the last couple of days here. Just curious if there's anything notable on safety. If you look at Acoramidis and Taf both look pretty clean. I'm just curious if there's anything -- anything there that you guys see that we should be?
Neil Kumar
Yes, I can take that and then come back to you for the question. Yes, I think to your point, both of these drugs are remarkably safe. We haven't seen this Dr. Gilmore suggested it anything that caused us concern. One of the things that's been interesting in patient ad for us is there was a bit of focus with tafamidis on the imbalance in falls and erectile dysfunction. Those are point estimates. So one does not know how important that, that might be. But on our study harmingly, that actually was reversed and the point has been favored treatment both in terms of fall and in terms of central interacts function.
Unknown Analyst
Okay. Got it. Neil. The other question I wanted to ask here up too. So just one just on Slide 14. We've gotten a few questions on this. It seems like the arms inverted on the all-cause mortality and then flipped back again. So it looks like they inverted kind of around month or so and then they flip back. Just curious what was the dynamic there that caused for that dynamic, I guess. And then on the last question here, on the time to improvement for anti-proBNP in the 6-minute walk, is there anything you can tell us for the patients that do see an improvement in those measures?
When did they improve and perhaps what was the mean improvement, if you can give us that information.
Neil Kumar
Do you want to take that?
Jonathan Fox
Yes, sure. Jonathan Fox here, Chief Medical Officer. I'll try to take a status to your question about can curves. So in order for the cost commercial habits model to hold to complete fidelity, the slopes of the lines would have had to be constant. And obviously, they're not -- they kind of -- they're steep sections and their relatively flat sections. And so if you were to, in a way, even though this would state be an appropriate thing to do. But in your mind, you could sort of redistributing all those deaths so that they happen at a more constant rate, so to speak.
And then those -- in order to flatten out those lines or pull them into a more of a constant slow and the final results, just the final result. One interesting aspect of this is that because of the lines crossed according to your correct observation, in fact, cost proportional has is model has been violated in terms of the assumptions that go into it, which is as the name of the test implies it assumes that the proportional hazards of the 2 different arms are, in fact, constant over the entire duration of the trial and obviously, they're not.
So the result is what it is. I mean everybody in this sort of endpoint analysis expects to see a KM curve according to cost course of hazards. But in fact, we did go back because of the assumptions not holding, we went back and apply a couple of other sensitivity analyses using some other nonparametric tests that yielded a consistent result is what I can say that.
Neil Kumar
Yes. Maybe just to build on that, I think you're referring to a few questions I also got from some investors about like could that be the action of the [indiscernible] dropping now it's a super low end current. So as Jonathan said, the data are the data, but there's nothing that you can ascribe to some action associated with drop and there's little levels of dropping, as you remember from our JPM comments around that time. And certainly, we don't actually at any time, see to fans on population outperforming the Acoramidis population in terms of mortality. What was your fist question again?
Unknown Analyst
On the question on NT-proBNP and 6-minute walk, given the notable improvement in a significant portion of the patients. Just curious when do these patients actually see that improvement at what time point? And in anti-probes -- and what would the mean or meeting whatever you can give us quantification of that improvement?
Neil Kumar
Yes. Both great questions. So I mean, interestingly, on 6-minute walk is obviously improvements were only shown once we had enough [indiscernible] on placebo, which obviously, we're well after last 12 months, as we all know. For the first quarter. And then on the second piece, you do see this immediate separation associated with [indiscernible] and KCCQ, which I think is quite our nano.
Jonathan Fox
Yes. Just one point of clarification. Those measures of improvement from baseline remain at 3 time points -- so obviously, it only applies to those people who made to 30. Got it. drops of debt for some of the reasons that were not included in that assessment.
Unknown Analyst
Understood Okay. Congrats again.
Operator
Our next question comes from Tyler Van Buren with TD Cowen.
Tyler Van Buren
Great. Gilmore, do you think Tafamidis would have shown similar results on mortality if tested in this exact same population? And as a follow-up to that, given the acceleration and separation of the mortality curves in the last 6 months, do you think it's possible that Acoramidis could show a greater long-term mortality benefit in the OLE than what tafamidis even showed an attract if we follow these patients another 6 to 12 months. And after those 2, just finally, I would love to hear early feedback from ESC from your colleagues what it's been like.
Unknown Executive
So I'll take the questions in reverse on the early impact from the EMC colleagues is extremely positive. And I think most people were are impressed by the data as they were. In terms of your second question, yes, I do think that we may see the survival, improving in terms of the open-label extension and potentially see survival that is better than that we see with Tafamidis. But as you already are aware, survival, the overall survival of 81% at 30 months is already better than anything that we've ever seen previously. And your third question was about whether we would if we treated patients in this -- if we treat patients with this group of patients to families, would we see the same results.
I certainly don't think, for example, we would see a statistically significant difference in all cause mortality alone. So what I'm essentially saying is one would -- I expect to see reasonably similar results, although as we've heard, it may well be that the results from the ATTRibute-CM would be better in the current net compared to fastille compared within the current population.
Operator
Our next question comes from Tom Shrader with BTIG.
Thomas Shrader
Kind of a related question to Dr. Gilmore. Based on what we've seen for tafamidis and Acoramidis, are most of your colleagues now believing these drugs are different? Is that very much in flux? What do you think the best data are that they are different. I think that it's a little bit early to say. I mean the principal of stabilization is 71 that colleagues are becoming increasingly aware of and the fact is that the principle of increased stabilization resulting in increased serum TTR resulting in increased benefit, if you see, I mean, that correlation in that relationship is something that, again, colleagues are becoming increasingly aware of.
Unknown Executive
So I think that, that provides powerful evidence, if you see what I mean, to the molecular mechanism for the benefits that we're seeing in this trial.
Thomas Shrader
Is that better than NT-proBNP in the minds of your colleagues?
Unknown Executive
I think they're very different. I mean NT-proBNP is a useful biomarker for looking at progression or otherwise of clinical disease, serum TTR a bit early to base a trial purely on the increase in serum TTR, but one can foresee that in several years' time, it might be the ore-based trial on TTR, the raise in serum TTR as an early indicator of TTR stabilization.
Thomas Shrader
Got it. And then a quick follow-up for Neil. It sounds like you're itching to do a head-to-head trial. If you did a head-to-head trial with 1,000 patients with what you know about the 2 drugs for 30 months, is that big enough? Or is it even bigger than that?
Neil Kumar
What endpoint?
Thomas Shrader
Clinical endpoints, cardiovascular hospitalization and mortality.
Neil Kumar
I mean from what we know, it would likely be slightly bigger than that in future were going to go on mortality and CVH. I think the key here is to and we continue to do this strong look at our data and try to identify some populations and endpoints whereby you can actually run the trial in a reasonable amount of time. We haven't determined precisely what that looks like. But as I said, we're engaged on that topic.
Operator
Our next question comes from Paul Choi with Goldman Sachs.
Kyuwon Choi
Congratulations to Neil and team on the study results again. My first question is for Dr. Gilmore, and I was wondering if you could share if you and any of your colleagues have thought about which particular patient populations, Acoramidis might be most beneficial in. I think one of the results that stand out is the benefit in the mutant population, which was not seen with Tafamidis. And so I was just wondering if you can maybe comment on how you and your colleagues maybe initially thinking about segmenting patients for the various therapies. And then I had a follow-up question.
Unknown Executive
And to be completely honest, one would want to give Acoramidis to all patients with ATTR amyloidosis at this stage, and it's a simple fact. I think that obviously, patients with hereditary ATTR amyloidosis and polyneuropathy one may want to consider the RNA interference therapeutics. But with -- for patients with ATTR amyloid cardiomyopathy, which constitutes the vast majority one would currently want to give that parameters to all of them regardless of stage regardless of genotype, that's how I would be thinking about it. Okay.
Kyuwon Choi
Great. And then for Neil and the team, can you maybe comment on how you're thinking about the shape of the label and what specific claims you'd be looking for? And then for the ex U.S. filings, in 2024. Are there any particular gating factors? Or is it just prioritizing the U.S. filing first?
Neil Kumar
Yes, I think good question. I'll be brief on that. In terms of label, obviously, that's what is ongoing, and we'll need to see what the discussions look like with the agency, but I think the label will look very similar to the cat label. I think if not exactly the same in terms of different numbers, but very similar we're talking about the impact on a combination of mortality and CVA should as Dr. Gilmore rates that we use impact on those 2-factor win ratio as well. So I think these things will be very similar. And yes, to your second question, it is just about we're a small team.
We're trying to know as quickly as possible to get this drug out to the U.S. markets, hopefully, sometime Q3 of next year, but we'll start to see what the regulatory turnaround looks like, and we want to model that as quickly as possible with an EMA filing sometime in 2024. I think it's important to note that -- and we're having Dr. Gilmore here we were extremely privileged to work very closely with a wide variety of sites in Europe. The dynamics of the trial and we kicked it off or such that we prioritize a broader and more international study than certainly the other sponsors have and so we see it as our responsibility in turn then typically the drug as quickly as possible to all of those geographies.
So they're working at. I don't think there'll be much of a gap between the two.
Kyuwon Choi
Congratulations again.
Operator
Our next question comes from Mani Foroohar with SVB Leerink.
Mani Foroohar
Congrats on the data. Obviously, a lot of questions around some of the key endpoints. I was hoping to get into a patient population a little bit. Are there differences in baseline characteristics or on how diligently these patients were following standard of care, compliance, et cetera, between those patients and with Tafamidis drop in, and those not any difference we should be looking at between those 2 populations, those who had dropped in those who didn't before we start drawing internal conclusions comparing Tafamidis versus Acoramidis, for example.
Neil Kumar
Yes. Not really, we haven't seen anything yet, and it's hard to do a super rigorous study when you have 16% or around that. But that looks pretty well out as you would expect from the rate of [indiscernible] that weren't working anything that was in terms of NYHA class or anyway, that would have biased those results. In terms of the overall patient population, it's not that Gilmore pointed out, it was a slightly healthier population given the staging criteria that we use as compared to the ATTRACT trial. But that was as expected from when we could enroll and then you also observe the [indiscernible] of Tafamidis on placebo versus [indiscernible] I think is important to know. And Jonathan, do you want to add anything?
Jonathan Fox
Yes. Just one other point to make that I think might contribute to a better understanding of your -- and to answer your question, the only thing we really could control was nobody was allowed to be on -- to drop in on Tafamidis up to 12 months. Beyond that, we had no control over who dropped in win during their journey to the trial they dropped in and how sick they might have been at the time they dropped in versus the randomization works a retinization, so things that happened later on in the trial became control.
Mani Foroohar
Great. That's helpful. And then one follow-up, a question I've gotten from a few different people is -- so you are guys, as you mentioned, a relatively lean team. How do you think about potential capital requirements to the launch, how do you think about partnering strategy? I know you talked about partnering our capital or addressing capital at the Analyst Day, essentially a royalty in January. How has your thinking evolved around supporting this launch and getting the most out of the strong getting it to the largest number of patients possible.
Neil Kumar
Yes, it's a great question, Mani, and I think at a high level, principles to apply to the question are twofold: number one, we want to work with and believe we can be the best owner of this compound. But if there are other parties that help us, for instance, getting internationally more quickly as we look greater access to patients that need it, we certainly all ears for that. And then secondly, on the context of capital, as you well know, we're also seeking the lowest cost of capital to continue to finance the company through this value clinic funds, which are several over the course of the next 24 months and not just limited even to this program in ATTR cardiomyopathy.
I think that being said, we think there's probably an incremental close to $600 million needed for us to finance to profitability. That's actually extraordinary because of the fact that this market is quite large in HTRCM the ramp to be quite quick. So we'll look at a variety of different things to layer in that capital over the course of the coming couple of years as we launch this product and get through the 3 other Phase IIIs we have going on in AH1, LGBTI and achondroplasia.
Operator
Our next question comes from Ellie Merle with UBS.
Eliana Merle
Congrats again on the data. Maybe for the cardiovascular hospitalization data, what proportion of the cardiovascular hospitalization events were from heart failure visits? And I guess how do you view the inclusion of the urgent heart failure visits is potentially affecting the comparison of your hospitalization results to Tafamidis where those were not included in their Phase III.
Jonathan Fox
Yes. So we haven't really dug into this data as deeply just yet as we'd like to. So I don't really have a firm answer for you today. Given the nature of the disease under study, you would expect most of them to partner of hospitalizations. And often, though, if they're triggered by new occidental tribulation, for example, that would be encoded as the reason for hospitalization, even though the need for hospitalization in the context of nuance, for example, is probably type coupled to the fact that these are people with heart failure. Someone with a normal heart who experiences an episode of it, they may well be treated in the emergency department and discharge to home.
So in the coming weeks and months, we will be digging into the details of those sorts of analysis and plan to publicize to in the future.
Eliana Merle
Sorry, I don't think I was clear just the urgent heart failure visit component of the CV hospitalization, sorry.
Jonathan Fox
You mean the events of clinical interest, those actually were a very, very small proportion of the total CDH, single-digit percent.
Eliana Merle
Okay. Great. That's helpful. And then just a follow-up. In the Class III patients, have you guys said what the breakdown was of the effect on survival in that subgroup?
Neil Kumar
No, we'll be releasing that and other classes and other analysis associated with the trial at AHA and other offices to come so didn't want to get it all the way to you
Operator
Our next question comes from Dane Leone with Raymond James.
Dane Leone
And thanks to Mani for asking the obligatory partnering question, so I don't have to. So the biggest debate coming out this weekend and that ESG is obviously the cross comparison to Tafa and how you guys position this product. And as you've said on the call, we don't have to rehash limits a cross trial comparison, especially something given this complexity. But what I do think is an important debate point that maybe we'll get answered at AHA and maybe you can opine on a little bit now, is with the ACM curve and some of the lack of stability in the proportional hazard ratio over the time course of the study.
There has been questions on when we see that time to first cardiovascular hospitalization curve is that going to look consistent throughout the study? And if it does, does it give you an angle of more comparability to attract in some form or fashion. If it doesn't, is that something that the clinical community is going to need additional data or explanation on and then finally, just in your view, is that the right cardiovascular metric to really be focused on when we're looking between the 2 studies and relative benefit rates.
Neil Kumar
Yes. I think [indiscernible] to first event is a great area to focus on. And I think stay tuned for AHA for more information on that. Yes. No, I do think, Dane, it's a really nice analysis to do, and I think it will help clinicians to understand the agents against each other. And I will emphasize that we are caveating all the stuff across to comparisons, which I think is important. And we see this as a large unmet need that we could work with several different sponsors on that at a conference just a couple of days before where large pharmacy was talking about the concept that typically is more sponsors come into space, especially in spaces under did.
And with this large enough need as this, the market just continues to grow and the opportunity to help patients continues to grow as well. So while we're focused on this being a more profound stabilizer, or equally focused I'm just trying to get a link field as quickly as possible and giving physicians a choice.
Operator
Our next question comes from Greg Harrison with Bank of America.
Greg Harrison
And congrats again on the data. So given that you've shown survival in cardio hospitalization rates approaching that of normal people in that age group, do you think you're nearing the limit of clinical benefit that could be achieved with the stabilization approach?
Neil Kumar
Yes. That is the point of doing the actuarial analysis to say what is possible. Our best guess is what the best drug can do is defensively to operate on the pathology of [indiscernible] and nothing else. So I agree with your premise that there's probably not a lot more headroom available. [indiscernible] The point is missing vary a little bit around here, but we're getting to the point here where it's -- it's very close to kind of what you can do.
Greg Harrison
Okay. Great. And then on the primary prevention trial, could you just talk a little bit more about the rationale there and how you would expect data from that trial to add to the profile of Acoramidis?
Jonathan Fox
Yes, Jonathan here. So we kind of have to kind of take 2 steps to the side here and cover a couple of important aspects of the study the patient population that we want to study. First of all, I just made a mistake called them a patient population that are not patients, they are asymptomatic carriers of pathogenic variance who are members of an identified family. And within the pedigree, there are affected family members who have developed for varying associated [indiscernible] test. And if you try to put yourself into the shoes of an individual obviously for the purposes of this discussion, a characteristic purchase in the trial would be depending on the variant and its associated age of onset.
It would be a young or middle panel and there by the objective criteria applied at screening, have no objective evidence of either of the polar opposite phenotypes or [indiscernible] type. But if you put yourself into that person attendance, they know that their carrier. They know that their first in-sector relatives have gone developed those gating progressive disease and they're frightened and they're worried. And many of them will come back every other year to the clinic to be evaluated. But then they're saying, well, I mean, why don't I have to wait until I hit symptomatic disease? Isn't there something you can do for me now?
To the point of the trial is to say, well, if we actually do take those people who are -- who have no evidence of disease who are presymptomatic and randomized and blinded therapy we had around placebo, can we, in fact, reduce or eliminate that onset of disease. So the endpoint is the development of objective criteria of either cardiomyopathy [ phoneropathy. ] And at that point, they would exit the trial and be invited to go to an open label extension. So if you fast forward to what's the goal here, the goal here is to develop a new indication that says Acoramidis is indicated for the prevention of ATTR any phenotype and variant carriers at risk.
Greg Harrison
Got it. That's helpful.
Operator
Our next question comes from Anupam Rama with JPMorgan.
Anupam Rama
Congrats on the update. And if I remember correctly, the Class III NYHA patients in the Tafamidis study ATTRACT didn't really show a favorable benefit in the subgroup analysis on CV hospitalization. But clearly, Acoramidis did on this subgroup analysis. Maybe for the company and Dr. Gilmore, like how do you put that data point into context of potentially population differences enrolled? As well as how that might impact your treatment practice decisions in more severe patients? And then the second question, Axis has been an issue with Tafamidis and hurdle to get to patients. Dr. Gilmore, maybe you can talk about have you ever had this experience in the U.K. or maybe what do your global colleagues expressed frustration with this and for the company remind us of how you're thinking about strategies to address the access concern?
Neil Kumar
Yes. I can frame it up and now I pass it over to Dr. Gilmore to handle this with expertise than I could. Yes, the point as that it's hardening in the right direction for Class III CDH, which was not observed as you mentioned, the ATTRACT trial. I will mention that the confidence interval does pass unit there. So the signals are consistently stronger as you go earlier in the sense what we see in the ATTRACT trial as well. But yes, it's great. It's one of the right way here. And maybe the last Dr. Gilmore can add anything?
Unknown Executive
At the point was heading in the right direction. I think this is probably a hyper power rather than the absence of efficacy necessary.
Neil Kumar
And then your second question was on access. I'll pass that over to -- do you have access to?
Unknown Analyst
We don't have access to firms in the U.K. and we are still in a situation where we don't have access
Anupam Rama
And for the company, how do you get -- what are your strategies to address the access concerns sort of in the U.S. and other regions?
Neil Kumar
Yes. So we've done a great deal of work on this. As we've said from the get-go, our goal really here is to provide access as broadly as possible, as quickly as possible. I think the hospitalization data and actually, the new pumps are new [indiscernible] help us to make the credible story, HTA authorities and we're working on story as well. But one is possible and try to gain access and all [indiscernible]. In the U.S., obviously, there's a change in dynamic associated with IRA.
And there's also much that can be done as we look at what other sponsors haven't done in terms of improving access and improving the physician's ability to write the drug for a patient and so we'll be employing some of those strategies that you've seen mostly in other therapeutic areas as we commercialize products.
Operator
Thank you. That's all the time we have for questions. I'd like to turn the call back over to Neil Kumar for any closing remarks.
Neil Kumar
All right. Well, thanks, everyone, for taking the time today. And as I mentioned, stay tuned for the data releases at AHA and in the months to come. Thanks again for your interest.
Operator
Thank you for your participation. This does conclude the program, and you may now disconnect. Everyone, have a great day.
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