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. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there will be a question and answer session. To ask a question, simply press star 1 on your telephone keypad. To withdraw your question, press star 1 again. It is now my pleasure to turn the call over to Brian Gerardo, 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 in future developments of Sarah Lutonin. These statements are subject to risks and uncertainties that could cause actual results to differ materially. Please refer to our SEC filings in today's press release for our 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, Fahim Hasning, Karen Peterson, Dr. Rob Bursigno. Additionally, we have Dr. Jean-Marie Brouille, Dr. Reiner Zimmerman, 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 three topics. First, a regulatory update, including our Type B pre-NDA meeting. Secondly, we will discuss results from our Procera CTFRI sub-study. 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 Fahim to discuss our recent progress.

Yeah, thanks. Thanks, Brian, and good morning, everybody. In February, we reported top-line results from Procera, our Phase III study of saralutinib in patients with PAH. At a high level, Procera showed a clinically meaningful placebo-adjusted improvement, of 13.3 meters and 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 pre-specified 0.025 alpha threshold. At the same time, all four key secondary endpoints favored seralutinib over placebo, and we saw a stronger effect in the pre-specified risk-enriched subgroup. Taken together, we believe the totality of the Procera data supports a real and clinically meaningful treatment signal. Now, since the Procera top-line readout, we've been focused on three work streams in parallel. First, we engaged with the FDA on the path forward for seralutin. 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. Karen will cover that in more details shortly. Second, we completed the analysis of the pre-specified CT-FRI sub-study, 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 was 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 seroludinib to patients. That included a significant reduction in force affecting approximately half the company, a sharp reduction in operating expenses as Procera 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 note holders to address the upcoming 2027 maturity. Brian 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 Procera, confirmatory data from Tori, multi-compartment mechanistic evidence from the CTFRI 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 and met need, and we believe we owe it to patients to pursue this path with discipline and urgency. I'll turn it over to Karen to discuss our regulatory interactions and next steps. Karen?

Thanks, Fahim. Let me start with 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 substantial evidence standard in place since 1998. For Gossamer, that approach is supported by the totality of the Phase III Procera data set together with the Phase II TORI study. We also believe the seriousness of PAH, the high unmet medical need, and Sarah Luton'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 Procera and TORI 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 within a defined timeline 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 Procera provides one adequate and well-controlled study, Tori 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 Brasigno to discuss the CTFRI sub-study findings. Rob?

Thank you, Karen. I will now spend the next few minutes walking through the Procera CTFRI sub-study and what it adds to our understanding of serolutinib's effect in PAH. So let's focus on what CTFRI adds to the Procera story. Clinical endpoints can tell us whether patients improved. FCT-FRI helps us understand the anatomical basis for that improvement. These analyses were performed with Fluida'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 serolutinib because it is not simply a vasodilator. Its mechanism is designed to address remodeling biology in the lung. In TORI, the FRI sub-study gave us an early hint that serolutinib could drive arterial reverse remodeling. The Procera sub-study was designed to go much deeper. It was a much larger, pre-specified, exploratory sub-study designed to test whether the TORI 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 sub-study 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 sub-study was balanced across arms and representative of the broader Procera Intent to Treat, or ITT, population on demographics, hemodynamics, and risk profile. The clinical endpoints in the sub-study were also consistent with the broader ITT population, including improvement in six-minute walk distance, NT-ProBNP, and RevealLight2. I'll walk you through what we found and why we think it matters. This slide gives the high-level result. Serolutinib showed statistically significant treatment effects across arterial, venous, and fibrosis-like parenchymal parameters. The CTFRI 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 Tori. Importantly, the imaging parameters correlated more tightly with clinical endpoints in Procera, including 6-minute walk distance, NT-ProBNP, and RevealLight2. The overall pattern is biologically coherent and consistent with serolutinib's inhibition of PDGFR, CSF1R, and CKIT. In other words, the findings form a coherent anatomical pattern that maps back to serolutinib's mechanism of action. So I want to point out that 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 CTFRI 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, CKIT, and its antiprolifitive, anti-inflammatory, and antifibrotic 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 CKIT inhibition map to reduced fibrosis-like parenchymal features. The parenchymal signal is important because it points to potential antifibrotic effects beyond vasodilatation. 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 serolutinib's mechanism of action. With that, I'll walk through each compartment individually. So, Procera 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 six-minute walk distance, NT-proBNP, reveal light 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 sub-study. 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 anti-fibrotic effect rather than a CTD-specific phenomenon. This signal is consistent with serolutinib's PDGFR, CSF1R, and CKIT biology and supports a potential effect on inflammatory and fibrotic remodeling distinct from vasodilatation. 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 serolutinib 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 Procera sub-study, the correlations support that connection. The tables at the bottom of this slide show at 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 six-minute walk distance, NT-ProBNP, and risk scores. These relationships were not detectable in the smaller Torrey sub-study. In Procera, 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, mid-sized 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 serolutinib'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 pre-specified exploratory substudy. The p-values are nominal and unadjusted for multiplicity. So to make the concept more tangible, this slide shows two 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 3 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 six-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, six-minute walk distance improved, and NT-ProBMP 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 seroluted 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 six-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 effects seen in the sub-study. 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 PHILD 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 breath 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 3 sub-study. In the parenchyma, serolutinib reduced fibrosis-like features supporting potential antifibrotic activity that is distinct from vasodilatation. In the vein, serolutinib 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 CKIT pathway inhibition. The clinical correlations are also important. These structural imaging findings correlated with improvements in six-minute walk distance, NT-pro-BMP, and Reveal-Lite 2. That links anatomical remodeling to clinical benefit. These data strengthen the cumulative weight of evidence for seralutinib across the program, including the placebo-controlled Phase I-B, the Phase II Tori study, and the Phase III Procera study. Taken together, we believe the CT-FRI data provide important anatomical support for the clinical benefit observed in Procera and reinforce seralutinib's differentiated profile on PAH. With that, I'll turn the call back over to Brian to discuss our financial position and recent capital structure actions.

Thanks, Rob. As of March 31st, 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 into the first quarter of 2027. Operating expenses will come down now that the Procera study has wound down. Additionally, we have implemented a reduction in force and broader cost containment measures. To this end, the first quarter included one-time charges, and our go-forward quarterly burn should be lower. I will leave the detailed financials to the press release and our 10Q 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 note holders since the Procera 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 first priority lien on substantially all the company's assets and bear cash interest at 7.5% paid semi-annually. 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. Kendra Fitzgerald is serving as dealer manager and Latham and Watkins is serving as our legal counsel. Additional details are included in the press release in our Form 8K that was filed with the SEC this morning. With that, let me turn it back over to Fahim for some closing remarks.

Thanks, Brian. 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 CTFRI 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 Procera data and the Phase II Tori data, we believe the overall evidence supports an NDA path for saraludna. So with that, Operator, we're ready to open the line for questions.

As a reminder, to ask a question, simply press star 1 on your telephone keypad. Again, that's star 1 to ask a question. And our first question comes from the line of Yasmeen Rahimi with Piper Sandler. Please go ahead.

Hi, this is Dominic on for Yasmeen Rahimi. Congrats on all the great updates in the Procera CTFRI 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?

Karen, we'll ask you to take that first part of that question.

Sure. Thank you, Fahim. 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 if we do get it in the label, it will be in the pharmacodynamics section of the label. Those discussions will occur at the meeting in June.

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

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.

Thank you so much.

Your next question comes from the line of Joseph Swartz with Leerink Partners. Please go ahead.

This is Heidi on for Joe. Thanks so much for taking our question. Can you walk us through the timeline between now and a potential September filing? What steps are getting to a potential NDA filing in addition to the Type B meeting? Karen yeah 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 you know late August so that we can get to 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 file in September.

And it's Brian, 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 advisors and consultancies that we've been using, that upon their review of the data, as well as the competitive landscape suggest that we should move aggressively forward because of the high 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.

Great. Thanks so much.

Your next question comes from the line of Ellie Morell with Barclays. Please go ahead.

Hi, this is Jasmine on for LE. Thank you for taking our questions, and congratulations on the data. I'm trying to understand the clinical relevance of these CTFRI measures. Is it common for physicians to do imaging like this when they manage these pH 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 subsidy have more imaging done at a later time point. Thanks.

Jean-Marie?

So, to answer the question, I think when we look at the standard endpoint, the PDR, the six-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 It provides a mechanistic insight. It separately quantifies 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 strengthens understanding of how CRHP works. So, we have a structural reverse remodeling versus acute vasodilatation. So, it's not a surrogate endpoint, I want to make sure of that, but it adds mechanistic credibility to support totality of evidence for regulators and clinicians. 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. um we will certainly be looking at uh the possibility of of repeating some of this imaging in uh at uh 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 he 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 Fluidia 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 three compartments having statistically significant effect, we think is not only very beneficial for patients, but is certainly setting a new standard for drugs in pulmonary to hypertension.

Great. Thanks so much. Your next question comes from the line of Camille DeVant with Guggenheim Securities. Please go ahead.

Great. Thanks for taking my questions. Maybe two if I could. So one, just curious in terms of communication 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 I'm trying, I guess there's a couple parts to the question. One, you mentioned that these patients in general seem to do similar to the patients in the broader study population at the clinical endpoint. Maybe you can provide a little bit more detail on that just in terms of the PVR, six-minute walk, you know, 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, Like, are there certain patient types or, you know, patient severities that you think may be better candidates for seralutinib than others based on the competitive dynamics out there, the other options that doctors have available?

Yeah, thanks for your question. Brown, you want to take the communication? Yeah, first piece.

Yeah. So, Vama, 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 Fahim, I'll let you direct the more important question for Vamo.

Yeah, Rob, 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 Procera intent-to-treat population. These patients did show significant improvement in six-minute walk and significant lowering or decrease in NT-pro-BMP, exactly what we would expect and very, if you will, supportive of this cohort. As far as your second question?

Yeah, well, I think the last part of your question was about commercial utilization and how would saralutinib 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 CTFRI 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.

Yeah, I think 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 Fahim said, because of what we're seeing from a safety and tolerability standpoint and efficacy standpoint now as imaging data, that we'll be able to stay on for a much longer time with that hopefully pretending, you know, better outcomes for these patients.

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

Okay. Thank you. Congrats on all the progress. Thank you, Bumil.

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

Yeah, thank you very much, and thanks all for listening in to the call. I just want to end this call by, first off, thanking the patients that participated in the Procera study. Obviously, without that participation, we're not able to advance treatments here for PAH. But 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.

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