Gossamer Bio, Inc. (GOSS) Q1 2026 Earnings Report, Transcript and Summary

Thank you for standing by. My name is Tina, and I will be your conference operator today. At this time, I would like to welcome everyone to the Gossamer Bio Q1 2026 Earnings Call. [Operator Instructions] It is now my pleasure to turn the call over to Bryan Giraudo, Chief Operating Officer and Chief Financial Officer. Please go ahead.

Good morning, and thank you for joining us. Before we begin, I'd like to remind listeners that today's discussion includes forward-looking statements, including statements regarding our regulatory plans, potential NDA submission and approval timing, commercialization, expectations, cash runway, capital structure and the potential therapeutic benefit and future developments of seralutinib. These statements are subject to risks and uncertainties that could cause actual results to differ materially. Please refer to our SEC filings and today's press release for discussions of these risks. We undertake no obligation to update these forward-looking statements, except as required by law. We are very excited this morning to have on our call today, Faheem Hasnain, Caryn Peterson, Dr. Rob Roscigno. Additionally, we have Dr. Jean-Marie Bruey, Dr. Rainer Zimmermann, Dr. Megan Flynn, Dr. Robin Osterhout; and Bob Smith, our Chief Commercial Officer, to speak about our exciting results this morning. Today, we plan to cover 3 topics: First, a regulatory update, including our Type B pre-NDA meeting; Secondly, we will discuss results from our PROSERA CT FRI substudy; and third, an update on our capital structure, including the convertible note exchange. Our financial results for the first quarter of 2026 are included in this press release, and I will come back to briefly discuss these at the end of the call. With that overview, let me hand it over to Faheem to discuss our recent progress. Faheem?

Yes. Thanks, Bryan, and good morning, everybody. In February, we reported top line results from PROSERA, our Phase III study of seralutinib in patients with PAH. At a high level, PROSERA showed a clinically meaningful placebo-adjusted improvement of 13.3 meters in 6-minute walk distance at week 24, with patients on seralutinib improving 28.2 meters from baseline versus 13.5 meters on placebo and a p-value of 0.032. That p-value met the traditional 0.05 threshold for statistical significance, but it did not meet the prespecified 0.025 alpha threshold. At the same time, all 4 key secondary endpoints favored seralutinib over placebo, and we saw a stronger effect in the prespecified risk-enriched subgroup. Taken together, we believe the totality of the PROSERA data supports a real and clinically meaningful treatment signal. Now since the PROSERA top line readout, we've been focused on 3 work streams in parallel. First, we engaged with the FDA on the path forward for seralutinib. That process advanced from the previously disclosed Type C meeting to a Type B pre-NDA meeting, which is the most formal pre-submission meeting type. The meeting has been confirmed as in person and the briefing book has been submitted. Caryn will cover that in more detail shortly. Second, we completed the analysis of the prespecified CT FRI substudy, which enrolled 162 patients with 125 evaluable paired scans at week 24. Those results showed multi-compartment structural reverse remodeling across arterial, venous, fibrosis-like and vascular complexity parameters. You will hear the full data shortly in the FRI section of the call. Third, we moved quickly on capital stewardship. We recognized immediately that while the top line results were clinically meaningful, it also created uncertainty, and we needed to act decisively to protect the company's financial position and preserve our ability to get seralutinib to patients. That included a significant reduction in force affecting approximately half the company, a sharp reduction in operating expenses as PROSERA winds down and the pause of other development activities and broader cost containment across the organization. At the same time, we engaged constructively with our convertible noteholders to address the upcoming 2027 maturity. Bryan will cover the outcome of that process later in the call. All of these actions were taken for the same reason, to make sure this company has the runway, the focus and the resources to pursue an NDA submission and ultimately get an approved treatment to patients with PAH. Our conviction in seralutinib has increased since the top line readout, not decreased. That conviction is based on the totality of evidence, consistent drug arm performance in PROSERA, confirmatory data from TORREY, multi-compartment mechanistic evidence from the CT FRI and the regulatory path we are advancing with the FDA. This is a first-in-class inhaled tyrosine kinase inhibitor for a rare and fatal disease with high unmet need, and we believe we owe it to patients to pursue this path with discipline and urgency. Now I'll turn it over to Caryn to discuss our regulatory interactions and next steps. Caryn?

Thanks, Faheem. Let me start with the regulatory pathway we are pursuing. We are pursuing an NDA submission under the framework of one adequate and well-controlled clinical investigation plus confirmatory evidence. This is consistent with FDA's recent guidance to articulate the flexibility in the amount and type of evidence needed to meet the substantial evidence standard in place since 1998. For Gossamer, that approach is supported by the totality of the Phase III PROSERA data set together with the Phase II TORREY study. We also believe the seriousness of PAH, the high unmet medical need and seralutinib's novel mechanism of action, complementary to existing PAH therapies all support this regulatory pathway. We plan to file the NDA based on the totality of the PROSERA and TORREY data sets and any adjustments to patient population will be guided by regulatory feedback. Turning to our engagement with FDA. We are now moving forward with a Type B pre-NDA meeting rather than a Type C initially under consideration. A Type B meeting is a formal pre-submission interaction with FDA where we provide an overview of the NDA in the form of a briefing book that FDA will provide written responses with a defined time line and formal meeting minutes. We submitted the meeting request in April 2026 and an in-person meeting has been granted by FDA and will be held in mid-June. Based on that timing, our NDA submission target remains in September this year, subject to the outcome of the pre-NDA meeting. If that process proceeds as expected, a potential approval could follow in the third quarter of 2027. So to summarize, we believe PROSERA provides one adequate and well-controlled study. TORREY provides the confirmatory evidence and the seriousness of the disease, the unmet medical need and the novel mechanism of action all support this NDA pathway. The Type B meeting is an important step in that process and supports our current NDA timing of September 2026. With that regulatory context in mind, I'll hand it over to Dr. Rob Roscigno to discuss the CT FRI substudy findings. Rob?

Thank you, Caryn. I will now spend the next few minutes walking through the PROSERA CT FRI substudy and what it adds to our understanding of seralutinib's effect in PAH. So let's focus on what CT FRI adds to the PROSERA story. Clinical endpoints can tell us whether patients improved. And CT FRI helps us to understand the anatomical basis for that improvement. These analyses were performed with Fluidda's functional respiratory imaging or FRI platform, which allows us to quantify anatomical changes in the pulmonary vasculature and surrounding lung parenchyma. That is especially important for seralutinib because it is not simply a vasodilator. Its mechanism is designed to address remodeling biology in the lung. In TORREY, the FRI substudy gave us an early hint that seralutinib could drive arterial reverse remodeling. The PROSERA substudy was designed to go much deeper. It was a much larger prespecified exploratory substudy designed to test whether the TORREY signal held up at scale and whether the effect extended beyond the arterial compartment. I want to acknowledge that this is the largest and most comprehensive CT FRI data set ever generated from a controlled therapeutic trial in pulmonary hypertension. A total of 162 patients enrolled in the substudy and 125 patients had paired baseline and week 24 CT scans available for analysis. These effects were observed on top of highly intensive background therapy, including patients receiving double, triple and quadruple PAH therapy. The substudy was balanced across arms and representative of the broader PROSERA intent-to-treat or ITT population on demographics, hemodynamics and risk profile. The clinical endpoints in the substudy were also consistent with the broader ITT population, including improvement in 6-minute walk distance, NT-proBNP and REVEAL Lite 2. I'll walk you through what we found and why we think it matters. This slide gives a high-level result. Seralutinib showed statistically significant treatment effects across arterial, venous and fibrosis-like parenchymal parameters. The CT FRI signal was not confined to one vascular compartment. The breadth and internal consistency of these effects go beyond the arterial-specific signal we first saw in TORREY. Importantly, the imaging parameters correlated more tightly with clinical endpoints in PROSERA, including 6-minute walk distance, NT-proBNP and REVEAL Lite 2. The overall pattern is biologically coherent and consistent with seralutinib's inhibition of PDGFR, CSF1R and c-KIT. In other words, the findings form a coherent anatomical pattern that maps back to seralutinib's mechanism of action. So I want to point out the patient image on the right side of this slide is illustrative, but it gives a first visual sense of what we mean by reverse remodeling. At a high level, you want to see more red appear than blue. We'll come back to this case a little later and go through it in more detail. So let's first discuss the pulmonary vasculature. To interpret the CT FRI findings, it helps to start with the biology. PAH affects an integrated vascular and parenchymal system. PAH has historically been treated as an arterial disease, but it is not only an arterial disease. The pathology involves arteries, the capillary bed, venous filling, inflammation and parenchymal remodeling around the vascular bed. Those compartments are connected. If the arteries are obstructed, the capillaries are underperfused, transpulmonary flow is reduced and the veins become underfilled, inflammation and fibrosis add to the problem throughout the system. So if a therapy is truly modifying disease biology upstream, you would expect downstream effects to move in a coherent direction as well. If you look at the right-hand side of this slide, you can see each pulmonary vascular compartment, its structure and function, how it is affected by disease in addition to calling out what CT can actually detect. So this next slide maps each target of seralutinib, PDGFR, CSF1R, c-KIT and its anti-proliferative, anti-inflammatory and anti-fibrotic effects to each compartment of the pulmonary vasculature where we would expect it to act and to the imaging signal we observed. Starting in the pulmonary arteries, PDGFR inhibition maps to the arterial reverse remodeling signal, including reduced large atrial blood volume proportion. Next, in the parenchyma, PDGFR, CSF1R and c-KIT inhibition map to reduced fibrosis-like parenchymal ProACT features. The parenchymal signal is important because it points to potential anti-fibrotic effects beyond vasodilation. Finally, in the veins, we see increased venous volume and branching, which we view as an integrated downstream readout of improved upstream arterial parenchymal and capillary bed biology. The key point is that each compartment moves in a direction that is consistent with seralutinib's mechanism of action. With that, I'll walk through each compartment individually. So PROSERA reproduced and extended the reverse remodeling signal we first saw in the TORREY study. In the figure on the right, seralutinib significantly reduced BV10A percentage, which measures large arterial blood volume as a proportion of total blood volume. That is consistent with proximal arterial decompression and blood volume redistribution away from larger remodeled proximal vessels towards smaller peripheral arteries. This is the compartment where we would expect PDGFR inhibition to show up most clearly. BV10A percentage also demonstrated among the strongest clinical correlations of any FRI parameter. Towards the bottom of the slide, we show these clinical correlations. Importantly, changes in this arterial parameter correlated with improvements in 6-minute walk distance, NT-proBNP, REVEAL Lite 2 and ESC/ERS risk. So this arterial signal is not only statistically significant, it is also clinically connected and consistent with the signal we first observed in the TORREY substudy. Next, we look at the parenchymal signal. This may be one of the more important new findings in this data set. In the figure on the right, seralutinib significantly reduced fibrosis-like parenchymal volume and also normalized fibrosis-like parenchymal volume, while placebo progressed. To our knowledge, this is the first demonstration of a statistically significant reduction in fibrosis-like parenchymal features in a controlled PAH trial. These measures are CT-derived imaging metrics. They are not histology, but they quantify voxel-level features characteristic of fibrotic tissue using a deep learning algorithm trained on confirmed IPF patient data sets analogous to high attenuation area or HAA approaches reported by Insmed. The reductions were consistent across subgroups, including non-CTD patients, which supports a broader anti-inflammatory and antifibrotic effect rather than a CTD-specific phenomenon. This signal is consistent with seralutinib's PDGFR, CSF1R and c-KIT biology and supports a potential effect on inflammatory and fibrotic remodeling distinct from vasodilation. Clinical correlations are noted at the bottom of the slide. One important point is that CT likely underestimates the full remodeling burden in PAH because much of this relevant perivascular and capillary bed biology occurs below the resolution of the CT. So the detectable reduction in fibrosis like parenchymal features may capture only part of the total remodeling effect. The same fibrotic and inflammatory pathobiology is also relevant to PH-ILD and other fibrotic lung diseases, which supports the potential relevance of seralutinib beyond PAH. Finally, the venous compartment then gives us an integrated view of how these upstream effects may translate into improved blood flow. Let's look at seralutinib's effects on the pulmonary veins. In the figure on the right, seralutinib significantly increased total venous blood volume while placebo decreased. Clinical correlations are noted on the bottom of the slide. We also saw consistent increases across venous vessel sizes and vascular branching, including fractal dimension. To our knowledge, this is the first demonstration of venous vascular recovery in a controlled PAH trial. Why does that matter? In PAH, venous underfilling reflects reduced transpulmonary flow. It is not primarily a venous disease. If upstream arterial obstruction, parenchymal remodeling and capillary bed impairment begin to improve, the downstream consequence should be improved venous filling. This is why we view the venous signal as more than another isolated parameter. It may be an integrated readout of the broader treatment effect upstream. The increase in venous branching is also important because it suggests improved vascular complexity, not simply passive volume redistribution. The next question is whether these anatomical changes relate to clinical trajectory. In the PROSERA substudy, the correlation support that connection. The tables at the bottom of this slide show a baseline arterial, venous and vascular complexity parameters correlated with hemodynamic and clinical measures, including pulmonary vascular resistance, mean pulmonary arterial pressure, cardiac output, NT-proBNP and risk scores. Changes in FRI parameters also correlated with improvements in 6-minute walk distance, NT-proBNP and risk scores. These relationships were not detectable in the smaller TORREY substudy. In PROSERA, the larger sample size and updated algorithm allowed us to see a stronger link between anatomical imaging findings and clinical outcomes. That gives us confidence that these are not just imaging observations. They are biologically and clinically relevant measures that help connect structural remodeling to clinical benefit. So this table pulls the compartment level findings together all in one place. In the arterial category, BV10A percentage decreased, consistent with reduced large artery blood volume proportion and proximal decompression. In the parenchymal category, both fibrosis-like parenchymal volume and normalized fibrosis-like parenchymal volume decreased. In the venous category, total venous blood volume, small venous blood volume, midsized venous blood volume and venous fractal dimension all increased. The key point here is not any single parameter in isolation. It's the consistency of the signal across arterial, parenchymal and venous measures. This pattern is what we would expect from seralutinib's mechanism, arterial reverse remodeling, reduced fibrosis-like parenchymal features and improved downstream venous filling and vascular branching. More broadly, the pattern is directionally supportive across the data set, including parameters that did not individually reach statistical significance. Again, I want to remind you this was a prespecified exploratory substudy. The p-values are nominal and unadjusted for multiplicity. So to make the concept more tangible, this slide shows 2 patient examples. These are individual patients, not the trial result, and they are not representative of the full study population. Both patients were on triple stable background therapy and were functional Class III at baseline. In the placebo case on the left, the patient remained on intensive background therapy, but the vasculature worsened over time. Total venous volume decreased, proximal arterial volume increased and 6-minute walk distance stayed essentially flat. Let's compare this to the seralutinib case on the right. I showed this image to you earlier. Here, we see the visual pattern we mean by reverse remodeling. Large arterial volume decreased, small arterial volume increased, total venous volume increased, 6-minute walk distance improved and NT-proBNP declined. The important point is that the visual pattern lines up with the population level data, arterial decompression, venous filling and clinical improvement, all moving together. This next example focuses specifically on the fibrosis-like parenchymal signal. The images on the left are from a single seralutinib-treated patient on double background therapy who had a visible reduction in fibrosis-like CT features from baseline to week 24. The patient also had improvement in 6-minute walk distance and NT-proBNP. The important point is not the individual patient alone. It is that the visual change is directionally consistent with the broader parenchymal treatment effect seen in the substudy. So fibrosis volume was quantified using FibroNet, a deep learning algorithm trained on confirmed IPF patient data and analogous to high attenuation area or HAA approaches used in ILD imaging. Again, CT only detects changes above a certain resolution. It likely understates the full burden of remodeling, particularly around the capillary bed. This supports the potential relevance of seralutinib in diseases where vascular remodeling, inflammation and fibrosis overlap, including PH-ILD and other fibrotic lung diseases. So to summarize, if we step back, PAH is a multi-compartment disease and seralutinib appears to affect these compartments in a coherent way even on top of intensive background therapy. The importance of these data is the consistency of the signal across anatomy, mechanism and clinical outcomes. Multi-compartment, vascular remodeling effects of this breadth have not been shown by traditional vasodilator therapies, which suggest added structural benefit rather than something redundant with existing vasodilator therapy. The arterial remodeling signal we first saw in the TORREY substudy is now reproduced and extended in a much larger Phase III substudy and the parenchyma seralutinib-reduced fibrosis-like features supporting potential anti-fibrotic activity that is distinct from vasodilation. In the vein, seralutinib showed what we believe is the first controlled trial evidence of venous vascular recovery, including gains in venous blood volume and branching. Taken together, these imaging signals point to a mechanism-based effect on disease biology consistent with PDGFR, CSF1R and c-KIT pathway inhibition. The clinical correlations are also important. These structural imaging findings correlated with improvements in 6-minute walk distance, NT-proBNP and Reveal Lite 2. That links anatomical remodeling to clinical benefit. These data strengthened the cumulative weight of evidence for seralutinib across the program, including the placebo-controlled Phase Ib, the Phase II TORREY study and the Phase III PROSERA study. Taken together, we believe the CT FRI data provide important anatomical support for the clinical benefit observed in PROSERA and reinforce seralutinib's differentiated profile in PAH. With that, I'll turn the call back over to Bryan to discuss our financial position and recent capital structure actions.

Thanks, Rob. As of March 31, 2026, we had cash and cash equivalents and marketable securities of $99 million. Based on our current plans, we expect our cash runway to extend to the first quarter of 2027. Operating expenses will come down now that the PROSERA study has wound down. Additionally, we have implemented a reduction in force and broader cost containment measures. To this end, the first quarter included onetime charges and our go-forward quarterly burn should be lower. I will leave the detailed financials to the press release and our 10-Q filing that we did on Friday afternoon. Moving on to the bond exchange. We have $200 million of aggregate principal amount convertible senior notes approaching maturity in 2027. With that maturity coming closer, addressing the capital structure proactively was a necessary step to keep the company focused on NDA execution and potential commercialization. We've been working constructively with our noteholders since the PROSERA top line readout in February, and both sides recognize the value of aligning the capital structure with the path forward as soon as practical. We were able to come to terms efficiently, and we view the outcome as an important step in removing the overhang and improving our focus on execution. Under the exchange for each $1,000 of existing notes tendered holders will receive a combination of equity consideration, new secured convertible notes and for those who tender early warrants. The new notes are secured by a priority -- first priority lien on substantially all the company's assets and bear cash interest at 7.5% paid semiannually. On a fully subscribed basis, this takes our outstanding convertible debt from $200 million down to $72 million, a reduction of $128 million and extends our debt maturity from 2027 to 2030. The exchange requires a minimum participation of 98%, which may be waived. We are also running a concurrent consent solicitation to remove substantially all restricted covenants from the existing indenture. Cantor Fitzgerald is serving as dealer manager and Latham & Watkins is serving as our legal counsel. Additional details are included in the press release and our Form 8-K that was filed with the SEC this morning. With that, let me turn it back over to Faheem for some closing remarks.

Thanks, Bryan. So stepping back, the key point today is that our conviction has strengthened. We've taken the balance sheet actions needed to align the company with a path forward. We now have a confirmed Type B pre-NDA meeting and expect to submit the NDA in September of 2026. We also have CT FRI data showing multi-compartment reverse remodeling across arterial, venous, fibrosis-like and complexity parameters with clinical correlations that support the biological relevance of those findings. Taken together with the Phase III PROSERA data and the Phase II TORREY data, we believe the overall evidence supports an NDA path for seralutinib. So with that, operator, we're ready to open the line for questions.

[Operator Instructions] And our first question comes from the line of Yasmeen Rahimi with Piper Sandler.

This is Dominic on for Yasmeen Rahimi. Congrats on all the great updates in the PROSERA CT FRI data. Could you help us understand how this data not only helps for the upcoming pre-NDA Type B meeting, but also potentially support a differentiated label? Kind of what are your thoughts on that and the plan with those data?

Yes. Caryn, we'll ask you to take the first part of that question.

Sure. Thank you, Faheem. The data that was presented today is going to go into the NDA. We did not get it in time to put it into the pre-NDA briefing package, although we will highlight it at the meeting. We believe it's going to be very important in terms of confirmatory evidence as we look at the biology and mechanistic plausibility. So the data set once fully complete, will be a big part of the NDA. And we -- if we do get it in the label, it will be in the pharmacodynamic section of the label. Those discussions will occur at the meeting in June.

And Bob Smith, can you handle the last part of the question around differentiation?

Sure. Absolutely. We feel like, first of all, the profile of seralutinib between the data in Phase I and Phase II is extremely strong. I think it even gets stronger with our Phase III data. With the FRI imaging data, this is unprecedented in the market. To my knowledge, we have not seen any other PAH therapy have this sort of information to clearly in humans show a strong reverse remodeling capability. And so we expect the label to be highly differentiated because of this.

Your next question comes from the line of Joseph Schwartz with Leerink Partners.

This is Heidi on for Joe. Can you walk us through the time line between now and a potential September filing? What steps are getting to a potential NDA filing in addition to the Type B meeting?

Caryn?

Yes, sure. We're actively working on the NDA submission as we speak. Obviously, it's a very large dossier and all of the analyses are ongoing and will be completed late August so that we can get the filing in mid-September. Everything is happening in parallel to the meeting, and we have been planning this for quite some time. So we're on track, and we'll be ready to file in September.

And it's Bryan. I would just add the following that the decision to go from a Type C to a Type B meeting, again, not only was on the basis of the totality of the evidence that we've seen through all of the clinical work with seralutinib, but at the recommendation of a number of our FDA advisers and consultancies that we have been using that upon their review of the data as well as the competitive landscape suggests that we should move aggressively forward because of the high unmet medical need. So again, I think it's very important that you take into consideration that it's not just Gossamer making this decision, but really robust support from those who have walked the walk, if you will, with the FDA within cardiorenal for many, many years.

Your next question comes from the line of Ellie Merle with Barclays.

This is Jasmine on for Ellie. Congratulations on the data. I'm trying to understand the clinical relevance of these CT FRI measures. Is it common for physicians to do imaging like this when they manage these PAH patients to measure progression or when diagnosing? And then secondly, would you expect the imaging results to deepen over time? And will patients in the substudy have more imaging done at a later time point?

Jean-Marie?

So to answer the question, I think when we look at the standard endpoint, the PVR, the 6-minute walk, the NT-proBNP, they measure the functional hemodynamic consequence of disease, but you don't visualize underlying structural change. So the clinical endpoint can be affected by placebo or background therapy. So what we have, the data we have with FRI, it provides a mechanistic insight. It separately quantify arterial, venous and fibrotic like feature and vascular complexity change. So we're trying to directly tie those markers with the disease pathology. I think the value is biological plausibility, FRI strengthen understanding of how seralutinib works. So we have a structural reverse remodeling versus acute vasodilation. So it's not a surrogate endpoint. I want to make sure that it does add mechanistic credibility to support totality of evidence for regulator and clinician. Concerning the questions at 48 weeks or 72 weeks, we don't have the data yet, but we will look into it.

And just to be clear, this technology is not something that's standard in the context of physician and clinical practice. But as what Jean-Marie said, is it really does bring the mechanistic evidence and the structural evidence to the table as to what seralutinib is doing in the context of the lungs. We will certainly be looking at the possibility of repeating some of this imaging in -- at later time points. And then obviously, when we have that data, we'll present it back to you.

And I think to add to what Faheem said, what's most important here -- I think what's most important here is no other sponsor has ever done this robust level of analysis using CT. So we do think that what Gossamer has achieved with this Fluidda CT study is going to set a new standard for how the community will look at a pharmaceutical intervention in PAH to see, as Rob laid out, all 3 compartments having statistically significant effect, we think is not only very beneficial for patients, but it's certainly setting a new standard for drugs in pulmonary artery hypertension.

Your next question comes from the line of Vamil Divan with Guggenheim Securities.

Maybe 2, if I could. So one, just curious in terms of communications post the meeting with the FDA. Should we assume to hear back sort of once you get the minutes, I don't know, I guess, maybe in the July sort of time frame or next updates we'd get from the company there. And then my other question is sort of tied to one of the earlier questions and just sort of based on the results here, I guess there's a couple of parts to the question. One, you mentioned that these patients in general seem to do similar to the patients in the broader study population on the clinical endpoint. Maybe you can provide a little bit more detail on that just in terms of the PVR 6-minute walk results you've seen with these patients. And I'm sort of curious what this means in terms of how you think about commercialization? Like are there certain patient types or patient severities that you think may be better candidates for seralutinib than others based on the competitive dynamics out there and the other options that doctors have available?

Bryan, do you want to take the first piece?

Yes. So Vamil, we'll provide an update on our FDA disclosures during our second quarter results that we'll do later in the summer after the meeting. But Faheem, I'll let you direct the more important question for Vamil.

Yes. Rob, do you want to handle the second piece?

So the second question, I believe, was how these patients, if you will, perform regarding their clinical endpoints as compared to the overall PROSERA intent-to-treat population. These patients did show significant improvement in 6-minute walk and significant lowering or decrease in NT-proBNP, exactly what we would expect and very if you will, supportive of this cohort. As far as your second question?

Yes. Well, I think the last part of your question was about commercial utilization and how would seralutinib get used in a commercial context. Bob, you can add in. But basically, clearly, you can see a very pronounced effect in the intermediate to high-risk subgroup. That's pretty clear. But the story doesn't end there. When you see the CT FRI data, you realize that something profound is going on in the context of the lung and even through the TORREY data, the ECHO data showing us what's going on in the right heart, that kind of so-called reverse remodeling context. I would like to tell you that the clinical community is quite intrigued about using this drug across the spectrum of patients because even in the lower-risk patients, the patients that are otherwise functionally quite capable, there is the potential to be able to use this drug earlier to prevent longer-term progression. And given the safety profile of the drug, not impact quality of life and that quality of life component becomes very important as you're using it in a patient that has otherwise pretty good functional capabilities. So we do see the potential for seralutinib to be used across the spectrum of PAH patients.

Yes. Faheem, that's exactly what I was going to say. I would just say with this data, I think it will motivate the market to start patients sooner on seralutinib. And as Faheem said, because of what we're seeing from a safety and tolerability standpoint and efficacy standpoint now as imaging data that they'll be able to stay on for a much longer time with that, hopefully portending better outcomes for these patients.

Yes. I don't think we can stress enough how important a new mechanism is for these patients, especially a new mechanism that doesn't carry the significant burden of toxicities that many of the current therapies do.

With no further questions in queue. I will now hand the call back over to Faheem Hasnain, CEO, for closing remarks.

Yes. Thank you very much, and thanks all for listening into the call. I just want to end this call by, first off, thanking the patients that participated in the PROSERA study. Obviously, without that participation, we're not able to advance treatments here for PAH. I'd also like to thank the patient advocacy groups that have been very supportive of Gossamer and the opportunity that seralutinib represents to their patients. And I want to thank the investigators and more broadly, the clinical community where we have been experiencing, I'm here at ATS now as we speak in Orlando, just the tremendous amount of support that we're getting and encouragement and quite frankly, the expectation that we will continue to push forward and get this drug approved. So thank you, everybody, and we look forward to further updates.

Thank you, again, for joining us today. This does conclude today's conference call. You may now disconnect.