Gossamer Bio, Inc. (GOSS) 2026 Q1 法說會逐字稿

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).

感謝您耐心等候。我叫 Tina，今天將擔任本次電話會議的接線員。此刻，我謹代表公司歡迎各位參加 Gossamer Bio 2026 年第一季財報電話會議。（接線員指示）。

It is now my pleasure to turn the call over to Bryan Giraudo, Chief Operating Officer and Chief Financial Officer. Please go ahead.

現在我很榮幸將電話交給營運長兼財務長 Bryan Giraudo。請開始。

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 to benefit in future developments of seralutinib.

各位早安，感謝各位加入我們。在開始之前，我想提醒各位聽眾，今天的討論包含前瞻性陳述，包括關於我們的法規計畫、潛在 NDA 申請與核准時程、商業化、預期、現金可支撐期間（cash runway）、資本結構，以及未來 seralutinib 開發可能帶來的效益等陳述。

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.

這些陳述受到各項風險與不確定性影響，可能導致實際結果與前述內容有重大差異。關於這些風險的討論，請參閱我們向 SEC 提交的文件以及今日的新聞稿。除法律要求外，我們不承擔更新這些前瞻性陳述的義務。

We were 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. Reiner Zimmerman, Dr. Megan Flynn, Dr. Robin Osterhout and Bob Smith, our Chief Commercial Officer. I'll just speak about our exciting results this morning. Today, we plan to cover three topics.

今天早上我們非常興奮能在電話會議上邀請到 Faheem Hasnain、Caryn Peterson、Rob Roscigno 醫師。此外，我們也有 Jean-Marie Bruey 醫師、Reiner Zimmerman 醫師、Megan Flynn 醫師、Robin Osterhout 醫師，以及我們的首席商務長 Bob Smith。我先簡要談談今天早上的令人振奮的結果。今天我們計畫涵蓋三個主題。

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 this at the end of the call.

第一，法規更新，包括我們的 Type B pre-NDA 會議。第二，我們將討論 PROSERA CT FRI 子研究的結果；第三，資本結構更新，包括可轉換公司債交換。我們 2026 年第一季的財務結果已包含在本新聞稿中，我會在電話會議結尾再簡要說明。

With that overview, let me hand it over to Faheem to discuss our recent progress. Faheem?

有了以上概述，接下來我把時間交給 Faheem，請他說明我們近期的進展。Faheem？

Yes. Thanks, Bryan, and good morning, everybody. In February, we reported top line results from PROSERA, our Phase 3 study of seralutinib in patients with PAH. At high level, PROSERA showed a clinically meaningful placebo-adjusted improvement of 13.3 meters in six-minute walk distance at week 24 and 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.

好的。謝謝你，Bryan，各位早安。2 月，我們公布了 PROSERA 的主要結果；PROSERA 是我們在 PAH 患者中評估 seralutinib 的第 3 期研究。整體而言，PROSERA 顯示在第 24 週時，六分鐘步行距離相較安慰劑經調整後有 13.3 公尺的具臨床意義改善；其中 seralutinib 組相較基線改善 28.2 公尺，安慰劑組改善 13.5 公尺，p 值為 0.032。該 p 值符合傳統 0.05 的統計顯著性門檻，但未達預先設定的 0.025 alpha 門檻。

At the same time, all four key secondary end points 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. And since the PROSERA top line readout, we've been focused on three work streams in parallel.

同時，四個關鍵次要終點皆顯示 seralutinib 優於安慰劑，且在預先指定的風險富集亞組中，我們觀察到更強的效果。綜合而言，我們相信 PROSERA 數據的整體證據支持一個真實且具臨床意義的治療訊號。自 PROSERA 主要結果讀出以來，我們同步聚焦於三條工作主軸。

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 presubmission 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.

第一，我們與 FDA 就 seralutinib 的後續路徑進行溝通。該流程已從先前揭露的 Type C 會議，推進至 Type B pre-NDA 會議，這是最正式的提交前會議類型。會議已確認為面對面進行，且簡報資料（briefing book）已提交。Caryn 稍後會更詳細說明。

Second, we completed the analysis of the prespecified CT FRI substudy, which enrolled 162 patients with 125 evaluable paired scans at week 24. We -- 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.

第二，我們完成了預先指定的 CT FRI 子研究分析；該子研究納入 162 名患者，其中第 24 週有 125 份可評估的配對掃描。我們——結果顯示在動脈、靜脈、類纖維化以及血管複雜度等參數上，出現跨多個區室的結構性逆向重塑。您將在本次電話會議的 FRI 段落中聽到完整數據。

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 seralutinib to patients. That included a significant reduction in force, affecting approximately half the company. sharp reduction in operating expenses as PROSERA winds down and the pause of other development activities and broader cost containment across the organization.

第三，我們迅速推動資本管理。我們立即意識到，雖然主要結果具有臨床意義，但也帶來不確定性，因此我們必須果斷行動，以保護公司的財務狀況並維持將 seralutinib 帶給患者的能力。這包括大幅裁員，影響約半數員工；隨著 PROSERA 逐步結束而大幅降低營運費用；暫停其他開發活動；以及在全組織推動更廣泛的成本控管。

At the same time, we engaged constructively with our convertible note holders 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.

同時，我們也以建設性的方式與可轉換公司債持有人溝通，以因應 2027 年到期的議題。Bryan 將在稍後的電話會議中說明該流程的結果。所有這些行動出於同一個原因。確保公司具備足夠的資金續航力、專注度與資源，以推進 NDA 申請，並最終為 PAH 患者帶來獲核准的治療。

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.

自主要結果讀出以來，我們對 seralutinib 的信心是增加而非降低。這份信心來自整體證據：PROSERA 中藥物組表現一致、TORREY 的確認性數據、CT FRI 所提供的跨多區室機轉證據，以及我們正與 FDA 推進的法規路徑。這是一款同類首創（first-in-class）的吸入式酪胺酸激酶抑制劑，用於一種罕見且致命、且未被滿足醫療需求極高的疾病；我們相信，我們有責任以紀律與緊迫感推進這條路徑，為患者努力。

I'll turn it over to Caryn to discuss our regulatory interactions and next steps. Caryn?

接下來我把時間交給 Caryn，請她說明我們的法規互動與後續步驟。Caryn？

Thanks, Faheem. Let me start with the regulatory pathway we are pursuing we are pursuing an NDA submission under the framework of 1 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.

謝謝你，Faheem。我先從我們正在推進的法規路徑談起：我們計畫在「1 項充分且良好對照的臨床試驗加上確認性證據」的框架下提交 NDA。這與 FDA 近期的指引一致，該指引闡明了自 1998 年以來「充分證據（substantial evidence）」標準下，在所需證據的數量與類型方面具有彈性。

We -- for Gossamer, that approach is supported by the totality of the Phase 3 PROSERA data set together with the Phase 2 TORREY study. We also believe the serious note of PAH, the high unmet medical need in seralutinib 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.

我們——對 Gossamer 而言，這一做法可由第 3 期 PROSERA 數據集的整體證據，結合第 2 期 TORREY 研究所支持。我們也相信，PAH 的嚴重性、seralutinib 所針對的高度未被滿足醫療需求，以及其新穎且可與現有 PAH 治療互補的作用機轉，都支持這條法規路徑。我們計畫基於 PROSERA 與 TORREY 數據集的整體證據提交 NDA，而任何對患者族群的調整將依據法規回饋來指引。

Turning to our engagement with FDA. We are now moving forward with the Type B pre-NDA meeting rather than a Type C initially under consideration. A Type B meeting is a formal presubmission interaction with FDA and 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.

接著談談我們與 FDA 的互動。我們目前將推進 Type B 的 pre-NDA 會議，而非先前考量的先行 Type C。Type B 會議是與 FDA 的正式提交前互動；我們會以簡報資料（briefing book）的形式提供 NDA 概覽，FDA 將在既定時程內提供書面回覆，並形成正式會議紀錄。我們已於 2026 年 4 月提交會議申請，FDA 已核准面對面會議，預計於 6 月中旬舉行。

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.

基於該時程，我們的 NDA 提交目標仍為今年 9 月，但仍取決於 pre-NDA 會議的結果。若該流程如預期推進，潛在核准可能於 2027 年第三季到來。

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.

總結而言，我們認為 PROSERA 提供了一項充分且良好對照的研究。TORREY 提供了確認性證據，而疾病的嚴重性、未被滿足的醫療需求以及新穎的作用機轉，皆支持此 NDA 途徑。Type B 會議是該流程中的重要一步，並支持我們目前 2026 年 9 月的 NDA 時程。

Without regulatory context in mind, I'll hand it over to Dr. Rob Roscigno to discuss the CT FRI substudy findings. Rob?

在不再延伸監管脈絡的前提下，我把時間交給 Rob Roscigno 醫師，請他說明 CT FRI 次研究的發現。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. CT FRI helps us understand the anatomical basis for that improvement.

謝謝你，Caryn。接下來幾分鐘，我將帶大家快速回顧 PROSERA 的 CT FRI 次研究，以及它如何加深我們對 seralutinib 在 PAH 中作用的理解。我們先聚焦 CT FRI 對 PROSERA 故事的增量價值。臨床終點可以告訴我們病人是否改善。CT FRI 則幫助我們理解這種改善背後的解剖學基礎。

These analyses were performed with Fluid as 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

這些分析是使用 Fluid 的功能性呼吸影像（functional respiratory imaging，FRI）平台完成，該平台可量化肺血管及其周邊肺實質的解剖變化。這對 seralutinib 尤其重要，因為它不僅僅是血管擴張劑。其機轉旨在處理肺部的重塑生物學。

In TORREY the FRI sub-study gave us an early hint that seralutinib could drive arterial reverse remodeling. The Proserasub study was designed to go much deeper. It was a much larger prespecified exploratory sub-study 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.

在 TORREY 中，FRI 次研究讓我們早期看到一個線索：seralutinib 可能促進動脈的逆向重塑。PROSERA 的次研究則被設計得更深入。這是一項規模更大、事先指定的探索性次研究，用以檢驗 TORREY 的訊號在更大樣本下是否仍成立，以及該效應是否延伸至動脈區室之外。我也想特別說明：這是迄今在肺高壓受控治療試驗中所產生、最大且最全面的 CT FRI 資料集。

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 PROSERA intent to treat or ITT population on demographics, hemodynamics and risk profile.

共有 162 名病人納入次研究，其中 125 名病人具備可供分析的成對基線與第 24 週 CT 掃描。這些效應是在高度密集的背景治療之上觀察到的，包括接受雙重、三重與四重 PAH 治療的病人。次研究在各治療組間分布均衡，且在人口學特徵、血流動力學與風險概況方面，能代表更廣泛的 PROSERA 意向治療（ITT）族群。

The clinical endpoints in the substudy were also consistent with the broader ITT population, including improvement in six-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 the 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 on TORREY.

次研究中的臨床終點也與更廣泛的 ITT 族群一致，包括六分鐘步行距離、NT-proBNP 與 REVEAL Lite 2 的改善。我將帶大家看我們發現了什麼，以及為何我們認為這很重要。這張投影片呈現高層次結果。Seralutinib 在動脈、靜脈以及類纖維化的肺實質參數上，皆顯示具統計顯著性的治療效果。CT FRI 的訊號並不侷限於單一血管區室。這些效應的廣度與內在一致性，超越了我們在 TORREY 首次看到的動脈特異性訊號。

Importantly, the imaging parameters correlated more tightly with clinical endpoints in PROSERA, including six-minute walk distance, NT-proBNP and REVEAL Lite 2. The overall pattern is biologically coherent and consistent with seralutinib 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 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.

重要的是，在 PROSERA 中，影像參數與臨床終點（包括六分鐘步行距離、NT-proBNP 與 REVEAL Lite 2）的相關性更為緊密。整體模式在生物學上是連貫的，且與 seralutinib 對 PDGFR、CSF1R 與 c-KIT 的抑制一致。換言之，這些發現形成一個一致的解剖學模式，並可回溯對應到 seralutinib 的作用機轉。因此我想指出，這張投影片右側的病人影像僅為示意，但它能讓大家初步直觀理解我們所說的逆向重塑。

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 printable system.

從高層次來看，你會希望看到紅色多於藍色。我們稍後會回到這個案例並更詳細地說明。接著先討論肺血管系統。要解讀 CT FRI 的發現，從生物學出發會更有幫助。PAH 影響的是一個整合性的血管與可列印系統。

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 printable remodeling around the vascular bit.

過去 PAH 常被視為動脈疾病，但它不僅是動脈疾病。其病理涉及動脈、毛細血管床、靜脈充盈、發炎，以及血管周邊的可列印重塑。

Those compartments are connected. If the arteries are obstructed, the capillaries are under perfused 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.

這些區室彼此相連。若動脈受阻，毛細血管灌流不足、經肺血流量下降，靜脈也會出現充盈不足。發炎與纖維化會在整個系統中加劇問題。因此，若某項治療確實在上游改變疾病生物學，你也會預期下游效應同樣朝一致方向變化。

If you look at the right-hand side of the 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.

如果你看投影片右側，可以看到每個肺血管區室、其結構與功能、疾病如何影響它，並且也標示出 CT 實際能偵測到的內容。

So this next slide maps each target of seralutinib, PDGFR, CSF1R, CCIT and its antiproliferative, 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 PDGFR pulmonary arteries, inhibition maps to the arterial reverse remodeling signal, including reduced large atrial blood volume proportion.

接下來這張投影片把 seralutinib 的各個標的（PDGFR、CSF1R、CCIT）及其抗增生、抗發炎與抗纖維化效應，對應到肺血管系統的各個區室：我們預期它作用的位置，以及我們觀察到的影像訊號。先從 PDGFR 的肺動脈開始，抑制作用對應到動脈逆向重塑訊號，包括大型心房血容量比例下降。

Next, in the parenchyma, PDGFR, CSF1R, and CCIT inhibition mapped to reduced fibrosis like parenchymal prat features. The parenchymal signal is important because it points to potential antifibrotic effects beyond basal dilitation. Finally, in the veins, we see increased venous volume in 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 mechanism of action.

接著在肺實質中，PDGFR、CSF1R 與 CCIT 的抑制對應到類纖維化的肺實質特徵降低。肺實質訊號很重要，因為它指向除基礎性擴張之外、可能存在的抗纖維化效應。最後在靜脈方面，我們看到靜脈容量與分支增加；我們將其視為上游動脈、肺實質與毛細血管床生物學改善後的整合性下游讀出。關鍵重點是：每個區室的變化方向都與 seralutinib 的作用機轉一致。

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 BV 10 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.

接下來，我將逐一說明各個分區。因此，PROSERA 重現並延伸了我們在 TORREY 研究中首次觀察到的逆向重塑訊號。在右側圖中，seralutinib 顯著降低 BV 10 百分比；該指標衡量大型動脈血容量占總血容量的比例。這與近端動脈減壓一致，並顯示血容量由較大、已重塑的近端血管重新分配至較小的周邊動脈。

This is the compartment where we would expect PDGFR inhibition to show up most clearly BV 10 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 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 sub study.

這個分區是我們預期 PDGFR 抑制最清楚呈現之處；BV 10 百分比也展現出在所有 FRI 參數中屬於最強的臨床相關性之一。在投影片下方，我們呈現這些臨床相關性。重要的是，該動脈參數的變化與六分鐘步行距離、NT-proBNP、REVEAL Lite 2 以及 ESC/ERS 風險的改善呈相關。因此，這個動脈訊號不僅具統計顯著性，也與臨床表現相連結，並與我們在 TORREY 子研究中首次觀察到的訊號一致。

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.

接著，我們看肺實質（parenchymal）訊號。這可能是此資料集中較重要的新發現之一。在右側圖中，seralutinib 顯著降低類纖維化的肺實質體積，並使類纖維化的肺實質體積趨於正常化，而安慰劑組則持續惡化。據我們所知，這是首次在受控的 PAH 試驗中，證實類纖維化肺實質特徵出現具統計顯著性的下降。這些量測為 CT 衍生的影像指標。

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.

它們不是組織學（histology），但會使用以已確認的 IPF 病患資料集訓練之深度學習演算法，量化體素（voxel）層級、具纖維化組織特徵的影像特徵；其方法類似 Insmed 所報導的高衰減區（high attenuation area，HAA）作法。

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 and CSR and CCIT biology and supports a potential effect on inflammatory and fibrotic remodeling distinct from vasodilation. Clinical correlations are noted at the bottom of the slide.

在各亞組中，下降幅度一致，包括非 CTD 病患，這支持其為較廣泛的抗發炎與抗纖維化作用，而非 CTD 特異現象。此訊號與 seralutinib 的 PDGFR 以及 CSR 與 CCIT 生物學一致，並支持其可能對發炎與纖維化重塑產生不同於血管擴張的作用。臨床相關性列於投影片下方。

One important point is that CT likely estimates 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.

一個重要重點是：CT 可能可估計 PAH 的整體重塑負荷，因為許多相關的血管周圍與毛細血管床生物學變化發生在 CT 解析度以下。因此，可偵測到的類纖維化肺實質特徵下降，可能僅反映總體重塑效應的一部分。相同的纖維化與發炎病理生物學也與 PH-ILD 及其他纖維化肺病相關，這支持 seralutinib 的潛在適用性可能不僅限於 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.

最後，靜脈分區提供我們一個整合視角，了解這些上游效應如何轉化為血流改善。我們來看 seralutinib 對肺靜脈的影響。在右側圖中，seralutinib 顯著增加總靜脈血容量，而安慰劑組則下降。臨床相關性列於投影片下方。我們也觀察到不同靜脈血管尺寸與血管分支（包括分形維度）均一致增加。

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.

據我們所知，這是首次在受控 PAH 試驗中證實靜脈血管恢復。這為何重要？在 PAH 中，靜脈充盈不足反映經肺血流（transpulmonary flow）降低。其主要並非靜脈本身的疾病。若上游動脈阻塞、肺實質重塑與毛細血管床受損開始改善，下游結果應是靜脈充盈改善。因此，我們將靜脈訊號視為不只是另一個孤立參數。

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.

它可能是對上游更廣泛治療效應的整合性讀出。靜脈分支增加也很重要，因為這暗示血管複雜度提升，而不僅是被動的血容量重新分配。

The next question is whether these anatomical changes relate to clinical trajectory and the PROSERA sub-study, the correlation 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.

下一個問題是：這些解剖學變化是否與臨床走勢相關？在 PROSERA 子研究中，相關性分析支持這種連結。本投影片下方的表格顯示，在基線時，動脈、靜脈與血管複雜度參數與血流動力學及臨床量測呈相關，包括肺血管阻力、平均肺動脈壓、心輸出量、NT-proBNP 與風險評分。FRI 參數的變化也與六分鐘步行距離、NT-proBNP 與風險評分的改善呈相關。

These relationships were not detectable in the smaller TORREY sub study. 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.

在樣本較小的 TORREY 子研究中，這些關係無法被偵測到。在 PROSERA 中，較大的樣本數與更新後的演算法使我們能看到解剖影像發現與臨床結局之間更強的連結。這讓我們更有信心：這些不只是影像觀察——它們是具有生物學與臨床意義的量測，有助於將結構性重塑與臨床獲益連結起來。因此，這張表將各分區層級的發現彙整於同一處。

In the arterial category, BV 10A percentage decreased consistent with reduced large artery, blood volume proportion and proximal decompression. In the parental 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.

在動脈類別中，BV 10A 百分比下降，與大型動脈血容量占比降低及近端減壓一致。在肺實質類別中，類纖維化肺實質體積與標準化的類纖維化肺實質體積皆下降。在靜脈類別中，總靜脈血容量、小靜脈血容量、中等大小靜脈血容量以及靜脈分形維度皆上升。

The key point here is not any single parameter in isolation. It's the consistency of the signal across arterial parental 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.

此處的關鍵不在於任何單一參數的孤立解讀。而在於動脈、肺實質與靜脈量測之間訊號的一致性。這種型態符合我們對 seralutinib 作用機轉的預期——動脈逆向重塑、類纖維化肺實質特徵降低，以及下游靜脈充盈與血管分支改善。更廣泛而言，整體資料集中呈現方向一致的支持性趨勢，包括部分單一參數未達統計顯著性的情況。

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 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 III at baseline.

再次提醒，這是一項預先規劃的探索性子研究。p 值為名目值，且未針對多重比較進行校正。因此——為了讓概念更具體，這張投影片展示兩個病患案例。這些是個別病患，而非試驗結果，且不代表整體研究族群。兩位病患在基線時皆接受三重且穩定的背景治療，功能分級為 III 級。

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.

左側安慰劑案例中，病患持續接受密集的背景治療，但血管狀況隨時間惡化。總靜脈容量下降、近端動脈容量上升，六分鐘步行距離基本持平。我們將其與右側 seralutinib 案例比較。我先前已向各位展示過這張影像。在此，我們看到我們所稱之逆向重塑的視覺型態。

Large arterial volume decreased, small arterial volume increased, total venous volume increased six-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 perancamal 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.

大型動脈血容量下降、小型動脈血容量上升、總靜脈血容量上升；六分鐘步行距離改善，且 NT-proBNP 下降。重點在於，視覺化圖樣與族群層級數據一致：動脈減壓、靜脈充盈與臨床改善同步發生。下一個例子將特別聚焦於類纖維化的肺實質訊號。左側影像來自一位接受 seralutinib 治療、並在雙重背景治療之上的單一患者；其類纖維化的 CT 特徵自基線至第 24 週可見下降。

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 effect seen in the substudy. So fibrosis volume was quantified using fibro net a deep learning algorithm trained on confirmed IPF patient data and analogous to high attenuation area or HAA approaches used in ILD imaging.

該患者的六分鐘步行距離與 NT-proBNP 亦有所改善。重點不僅在於單一個案。而是視覺變化的方向性，與子研究中觀察到的更廣泛肺實質治療效應一致。因此，我們使用 fibro net（以已確認之 IPF 患者資料訓練的深度學習演算法）量化纖維化體積；其方法類似於 ILD 影像中使用的高衰減區（HAA）等作法。

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.

同樣地，CT 只能偵測到高於某一解析度門檻的變化。它很可能低估了重塑的整體負荷，特別是在毛細血管床周邊。這支持 seralutinib 在血管重塑、發炎與纖維化重疊的疾病中可能具有相關性，包括 PH-ILD 及其他纖維化肺部疾病。

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.

總結而言，若我們退一步看，PAH 是一種多區室疾病，而 seralutinib 似乎能以一致且連貫的方式影響這些區室，即使是在強化背景治療之上亦然。這些數據的重要性在於，其訊號在解剖、機轉與臨床結果之間具有一致性。

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.

如此廣泛的多區室血管重塑效應，傳統血管擴張治療尚未顯示；這暗示其帶來的是額外的結構性效益，而非與既有血管擴張治療重複。

The arterial remodeling signal we first saw in the TORREY sub study has now reproduced and extended in a much larger Phase 3 sub-study. And the parenchymal seralutinib reduced fibrosis like features supporting potential antifibrotic activity that is distinct from vasodilation.

我們最初在 TORREY 子研究中看到的動脈重塑訊號，如今已在更大規模的第 3 期子研究中再現並延伸。此外，在肺實質方面，seralutinib 降低了類纖維化特徵，支持其可能具有不同於血管擴張作用的抗纖維化活性。

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 CCIT pathway inhibition.

在靜脈方面，seralutinib 顯示了我們認為是首個受控試驗中關於靜脈血管恢復的證據，包括靜脈血容量與分支增加。綜合而言，這些影像訊號指向一種以機轉為基礎、作用於疾病生物學的效應，與 PDGFR、CSF1R 與 CCIT 路徑抑制一致。

The clinical correlations are also important, these structural imaging findings correlated with improvements in six-minute walk distance, NT-proBNP 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 1b, the Phase 2 TORREY study and the Phase 3 PROSERA study.

臨床相關性同樣重要：這些結構性影像發現與六分鐘步行距離、NT-proBNP 與 REVEAL Lite 2 的改善相關。這將解剖性重塑與臨床獲益連結起來。這些數據強化了整體研發計畫中對 seralutinib 的累積證據力，包括安慰劑對照的第 1b 期、第 2 期 TORREY 研究，以及第 3 期 PROSERA 研究。

Taken together, we believe the CT FRI data provide important anatomical support for the clinical benefit observed in PROSERA and reinforced seralutinib 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.

綜合而言，我們認為 CT FRI 數據為 PROSERA 中觀察到的臨床獲益提供了重要的解剖學支持，並進一步強化 seralutinib 在 PAH 的差異化特徵——接下來我把電話交回給 Bryan，請他說明我們的財務狀況與近期資本結構措施。

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 into the first quarter of 2027. The operating expenses will come down now that the PROSERA study has wound down. Additionally, we have implemented a reduction in force in broader cost containment measures. To this end, the first quarter included onetime charges and our go-forward quarterly burn should be lower.

謝謝，Rob。截至 2026 年 3 月 31 日，我們持有的現金及約當現金與有價證券為 9,900 萬美元。依據我們目前的計畫，我們預期現金可支撐至 2027 年第一季。隨著 PROSERA 研究告一段落，營運費用將下降。此外，我們已實施裁員並採取更廣泛的成本控管措施。因此，第一季包含一次性費用，而未來每季的現金消耗（burn）應會較低。

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 of convertible senior notes approaching maturity in 2027.

更詳細的財務資訊我將留給新聞稿與我們於週五下午提交的 10-Q 申報文件。接著談債券交換。我們有總本金 2 億美元的可轉換優先票據，將於 2027 年到期。

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.

隨著到期日逼近，主動處理資本結構是必要步驟，以使公司能專注於 NDA 的執行與潛在商業化。自 2 月 PROSERA 主要結果公布以來，我們一直與票據持有人進行具建設性的合作；雙方都認同，應在可行的情況下儘快使資本結構與未來路徑一致。我們得以有效率地達成條件，我們也將此結果視為移除壓力來源並提升執行專注度的重要一步。

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.

依交換條款，每交付（tender）面額 1,000 美元的既有票據，持有人將獲得由股權對價、新的有擔保可轉換票據，以及（對於提前交付者）認股權證所組成的組合。新票據以公司幾乎所有資產作為擔保，並享有優先順位——第一順位留置權（first priority lien），且以 7.5% 現金利率計息、每半年支付一次。

On a fully subscribed basis, this takes our outstanding convertible debt from $200 million down to under $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.

在全數認購的情況下，我們未償可轉換債務將由 2 億美元降至低於 7,200 萬美元，減少 1.28 億美元，並將債務到期日由 2027 年延長至 2030 年。本次交換要求最低參與率為 98%，但該要求可能被豁免。我們也同步進行同意徵求（consent solicitation），以移除既有契約（indenture）中幾乎所有限制性條款（restricted covenants）。

Candrian shareholders serving as dealer manager and Nathan 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.

Candrian 股東擔任交易管理人（dealer manager），Nathan Watkins 擔任我們的法律顧問。更多細節載於新聞稿以及我們今早向 SEC 提交的 Form 8-K。

With that, let me turn it back over to Faheem for some closing remarks.

接下來，讓我把電話交回給 Faheem 做一些結語。

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.

謝謝，Bryan。回到整體來看，今天的關鍵重點是：我們的信心更強了。我們已採取必要的資產負債表措施，使公司與前進路徑一致。我們現在已確認 Type B 的 NDA 前會議，並預期於 2026 年 9 月提交 NDA。我們也有 CT FRI 數據顯示，在動脈、靜脈、類纖維化與複雜度等參數上出現多區室的逆向重塑，且與臨床指標相關，支持這些發現的生物學相關性。

Taken together with the Phase 3 PROSERA data and the Phase 2 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.

結合第 3 期 PROSERA 數據與第 2 期 TORREY 數據，我們相信整體證據支持 seralutinib 的 NDA 申報路徑。那麼，接線員，我們準備開放提問。

(Operator Instructions) Yasmeen Rahimi, Piper Sandler.

(接線員指示) Yasmeen Rahimi，Piper Sandler。

This is Dominic on for Yasmeen (inaudible). 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?

我是 Dominic，代替 Yasmeen(聽不清)。恭喜 PROSERA CT FRI 數據有這麼多重大更新。能否協助我們理解，這些數據如何不僅有助於即將到來的 pre-NDA Type B 會議？同時也可能支持一個具差異化的標籤（label）？想請教你們對此的看法以及這些數據的規劃是什麼？

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

好的。Caryn，我們先請你回答這個問題的第一部分？

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.

當然。謝謝你，Faheem。今天呈現的數據將會納入 NDA。我們沒有及時取得這些數據以放入 pre-NDA 簡報資料包（briefing package），不過我們會在會議上重點提及。我們相信，當我們檢視生物學與機轉可行性（mechanistic plausibility）時，這些數據在作為確認性證據（confirmatory evidence）方面將非常重要。

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, will be in the pharmacodynamic section of the label, those discussions will occur at the meeting in June.

因此，這套數據在完全完成後，將會是 NDA 的重要組成部分。而且——我們——如果能把它寫進標籤（label），會放在標籤的藥效學（pharmacodynamic）章節；相關討論將在六月的會議上進行。

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

另外，Bob Smith，你能否回答最後一部分、關於差異化的問題。

Sure. Absolutely. We feel like, first of all, the profile of seralutinib between the data, the Phase 1 and Phase 2 is extremely strong. I think it even gets stronger with our Phase 3 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.

當然。絕對可以。我們認為，首先，seralutinib 的整體特徵（profile）——綜合這些數據、第一期與第二期——非常強勁。我認為，隨著我們第三期的 FRI 影像數據，這個特徵更是進一步強化；這在市場上是前所未見的。據我所知，我們尚未看到任何其他 PAH 治療能在人體中如此清楚地提供這類資訊，顯示強勁的逆向重塑（reverse remodeling）能力——因此我們預期標籤會因為這點而高度差異化。

Joseph Schwartz, Leerink Partners.

Joseph Schwartz，Leerink Partners。

This is Heidi on for Joe. 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?

我是 Heidi，代替 Joe。你們能否帶我們梳理一下從現在到可能在九月申報（filing）的時間線？除了 Type B 會議之外，為了達成可能的 NDA 申報，還有哪些步驟？

Caryn?

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.

好的，當然。我們正在積極進行 NDA 送件準備。顯然這是一份非常龐大的申請資料（dossier），而且——所有分析都在進行中，並將在八月下旬完成，以便我們能在九月中旬完成申報。所有工作都與會議並行推進，我們也已規劃相當長一段時間。所以我們進度如期，並會準備好在九月送件。

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'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 unmet medical need.

我是 Bryan。我想補充的是——我們把會議從 Type C 改為 Type B 的決定，再次強調，不僅是基於我們在 seralutinib 所有臨床工作中看到的整體證據（totality of the evidence），也是在多位我們合作的 FDA 顧問與顧問公司建議之下；他們在審視數據以及競爭格局後，認為基於高度未被滿足的醫療需求（high unmet medical need），我們應該更積極地推進。

So again, I think it's very important that you take into consideration that it's not just Gossamer making a decision, but really robust support from those who have walked the walk, if you will, with the FDA within cardiorenal for many, many years.

所以再次強調，我認為非常重要的一點是，你們要考量這不只是 Gossamer 自己做的決定，而是來自那些多年來在心腎領域（cardiorenal）與 FDA「走過流程」的人所提供的非常強力支持。

Ellie Merle, Barclays.

Ellie Merle，Barclays。

This is Jasmeen on for Ellie. Congratulations on the data. I'm trying to understand the clinical relevance of these CT FRI measures -- is it common for a physician to do imaging like this when they manage these patients to measure progression or win 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?

我是 Jasmeen，代替 Ellie。恭喜你們的數據。我想了解這些 CT FRI 指標的臨床相關性——醫師在管理這些病人時，常見會做這類影像檢查來衡量疾病進展或用於診斷嗎？其次，你們預期影像結果會隨時間而更明顯嗎？而且在補貼研究（substudy）中，病人是否會在較晚的時間點再做更多影像檢查？

So to answer the question, I think when we look at the standard endpoint, the P, the six-minute walk, the NT-proBNP, the merger, 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, provides a mechanistic insight. It separately quantifying arterials and fibrotic light feature and vascular complexity chain.

針對這個問題，我認為當我們看標準終點，例如 P、六分鐘步行、NT-proBNP、合併終點（merger）、以及疾病的功能性血流動力學後果時，你並不會把底層的結構性改變視覺化。因此臨床終點可能會受到安慰劑或背景治療的影響。而我們用 FRI 所得到的數據，提供了機轉層面的洞見。它能分別量化動脈與纖維化的光學特徵，以及血管複雜度鏈（vascular complexity chain）。

So we are trying to directly tie those markers with the disease pathology. I think the value is biological plausibility, FRI strengthened understanding of how oceanic works -- so we have a structural reverse remodeling versus acute vasodilatation. So it's not a surrogate end point. I want to make sure that best add mechanistic credibility to support totality of evidence for regulatory and clinician. Concerning the questions at 48 weeks of 72 weeks, we don't have the data yet, but we will look into it.

因此我們試圖把這些標記直接與疾病病理連結起來。我認為其價值在於生物學可行性；FRI 強化了我們對 oceanic 如何作用的理解——因此我們看到的是結構性的逆向重塑，而不是急性血管擴張。所以它不是替代性終點（surrogate end point）。我想確保的是，這些結果能增加機轉可信度，以支持監管機關與臨床醫師所需的整體證據。至於 48 週或 72 週的問題，我們目前還沒有數據，但我們會進一步評估。

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.

另外要說清楚的是，這項技術在醫師與臨床實務中並不是標準作法。但如 Jean-Marie 所說，它確實把機轉證據與結構性證據帶到檯面上，說明 seralutinib 在肺部情境下正在做什麼。——我們也一定會評估在——較晚時間點重複進行部分影像檢查的可能性。然後當我們有了那些數據，會再向各位回報。

And I think to add to what Fehi said was most important here. I think what's most important here is no other sponsor has ever done this robust level of analysis using CT.

我想補充 Fehi 所說、這裡最重要的一點。我認為最重要的是，過去沒有任何申辦方曾用 CT 做到如此強健（robust）層級的分析。

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 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 it's certainly setting a new standard for drugs in pulmonary to her pretension.

因此我們確實認為，Gossamer 透過這項 Fluidda CT 研究所達成的成果，將為社群建立一個新的標準：在 PAH 的藥物介入上，如何檢視——如 Rob 所闡述——三個區室（compartments）皆呈現具統計顯著性的效果；我們認為這不僅對病人非常有利，也確實正在為肺高壓（pulmonary hypertension）領域的藥物樹立新的標準。

Vamil Divan, Guggenheim Securities.

Vamil Divan，Guggenheim Securities。

Maybe two, if I could. So one, just curious in terms of communications post the meeting with the FDA, should we assume that you're 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 1 of the earlier questions. And just based on the results here, I guess there's a couple of parts to the question.

如果可以的話，可能有兩個。第一個，我只是好奇在與 FDA 會議之後的溝通安排，我們是否可以假設一旦你們拿到會議紀要，就會再度對外更新？我不確定，我想可能是在 7 月左右的時間點，或是公司下一次對外更新會在那時候。然後我的另一個問題有點呼應先前其中一個問題。就基於這裡的結果來看，我想這個問題有幾個部分。

One, you mentioned that these patients in general seem to do similar to the patients and the broader study population on the clinical endpoint. Maybe you can provide a little bit more detail on that just in terms of PVR six-minute walk results you've seen with these patients?

第一，你提到這些患者整體而言在臨床終點上的表現，似乎與更廣泛研究族群中的患者相近。你是否可以就此提供更多細節，特別是就你們在這些患者身上看到的 PVR 與六分鐘步行測試結果？

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 a build --

另外我也有點好奇，這對你們如何思考商業化意味著什麼；例如，基於外部競爭態勢以及醫師可用的其他選項，你們是否認為某些患者類型或疾病嚴重程度的患者，可能比其他人更適合作為 seralutinib 的候選人？--

Bryan, do you want to take the community yes, first piece?

Bryan，你要先回答社群那個、對，第一部分嗎？

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 him, I'll let you direct the more important question for Vamil.

好的，所以 Vamil，我們會在第二季財報結果電話會議中，提供我們與 FDA 溝通揭露事項的更新；那會是在會議之後、夏季稍晚的時間。不過，較重要的問題我就讓你引導 Vamil 來回答。

Yes. Rob, do you want to handle the second set.

好的。Rob，你要處理第二組問題嗎？

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

我認為第二個問題是：這些患者在臨床終點上的表現，與整體意向治療（intent-to-treat）族群相比如何。這些患者在六分鐘步行距離上確實顯示顯著改善，NT-proBNP 也顯著下降或降低，完全符合我們的預期，也非常支持這個隊列的結果。至於你的第二個問題呢？

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.

好的。我想你問題的最後一部分是關於商業化使用情境，以及 seralutinib 在商業環境中會如何被使用。Bob，你也可以補充。但基本上，很明顯你可以看到在中度到高風險亞組中有非常顯著的效果。這點相當清楚。

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.

但故事不只如此。當你看到 CT FRI 的數據時，你會意識到在肺部的脈絡下有一些深刻的變化正在發生；甚至從 TORREY 的數據、ECHO 的數據也顯示右心正在發生的變化，也就是所謂的逆向重塑（reverse remodeling）的脈絡。

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.

我想告訴你，臨床社群對於在各類患者光譜中使用這個藥物相當感興趣；因為即使在較低風險的患者、也就是功能上其實相當良好的患者身上，也有可能更早使用此藥，以預防長期疾病進展——而且考量到此藥的安全性特徵，不會影響生活品質。

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.

而當你把它用在原本功能能力就相當不錯的患者身上時，生活品質這個面向就變得非常重要。因此，我們確實看到 seralutinib 有潛力可用於整個 PAH 患者光譜。

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 is imaging data that will be able to stay on for a much longer time with that, hopefully, pretending better outcomes for these patients.

是的，Faheem，這正是我想說的。我只想說，憑藉這些數據，我認為會促使市場更早讓患者開始使用 seralutinib。而且如 Faheem 所說，基於我們在安全性與耐受性以及療效方面所看到的結果，再加上現在的影像數據，患者將能夠用藥更長時間；希望這能預示這些患者會有更好的結局。

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.

是的。我認為我們再怎麼強調都不為過：對這些患者而言，一個新的作用機轉有多麼重要，尤其是這種新的作用機轉不會像許多現有療法那樣帶來顯著的毒性負擔。

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

目前佇列中沒有其他問題。我現在把電話交回給執行長 Faheem（聽不清楚）做結語。

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. 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.

好的。非常感謝，也謝謝各位收聽本次電話會議。我想在結束前，首先感謝參與 PROSERA 研究的患者。顯然，沒有他們的參與，我們就無法推動 PAH 的治療進展。同時我也要感謝一直以來非常支持 Gossamer 的病友倡議團體，以及 seralutinib 對其病友所代表的機會。

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 an encouragement -- and quite frankly, the expectation that we will continue to push forward and get this drug approved.

我也要感謝研究者，以及更廣泛的臨床社群；我們一直感受到——我此刻正在奧蘭多參加 ATS——我們獲得了大量的支持與鼓勵——坦白說，也有一種期待：我們會持續推進並讓這個藥物獲得核准。

So thank you, everybody, and we look forward to further updates. Thank you.

所以謝謝大家，我們也期待後續更多更新。謝謝。

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

再次感謝各位今天加入我們。本次電話會議到此結束。您現在可以掛線。