ALX Oncology Holdings Inc (ALXO) 2026 Q1 法說會逐字稿

Greetings, and welcome to the ALX Oncology first-quarter 2026 financial results conference and webcast. (Operator Instructions) Please note, this conference is being recorded.

各位好，歡迎參加 ALX Oncology 2026 年第一季財務業績電話會議與網路直播。(接線員指示) 請注意，本次會議將被錄音。

I will now turn the conference over to your host, Jason Lettmann, CEO. Please go ahead, sir.

現在我將把會議交給各位的主持人、執行長 Jason Lettmann。先生，請開始。

Thanks, everyone, and welcome to our Q1 2026 results. I really appreciate you all spending time with us this morning and are looking forward to sharing these updates with you. On slide 2 and before we start our presentation as housekeeping, here are our forward-looking statements for your review. On slide 3, here's the agenda and plan for today. We're going to be providing an update on our key accomplishments in the first-quarter of 2026.

謝謝各位，歡迎參加我們 2026 年第一季（Q1）業績說明。非常感謝大家今天早上撥冗與會，我們也期待與各位分享最新進展。在投影片第 2 頁，在我們開始簡報之前，先請各位參閱我們的前瞻性聲明，作為例行事項。投影片第 3 頁是今天的議程與安排。我們將提供 2026 年第一季關鍵里程碑的最新進度。

Most notably, we are very excited to share with you the data set that was presented yesterday in Munich at ESMO Breast 2026 from the analysis of our trial evaluating evorpacept and zanidatamab, which clearly showed again that CD47 expression is a key predictive biomarker for increasing durable clinical response in heavily pretreated HER2-positive patients.

最值得一提的是，我們非常興奮與各位分享昨天在慕尼黑 ESMO Breast 2026 發表的資料集，該資料來自我們評估 evorpacept 與 zanidatamab 的試驗分析，結果再次清楚顯示：在接受過多線治療的 HER2 陽性患者中，CD47 表現量是提升持久臨床反應的重要預測性生物標誌。

This further validates the results we saw with Evo and HER2-positive gastric cancer from our ASPEN-6 trial. We are also very excited today to be joined by Dr. Sara Hurvitz from the Fred Hutch Cancer Center at the University of Washington, who is a well-recognized expert in metastatic breast cancer. She will be presenting the ESMO breast data in detail and also share her views on evorpacept's significant potential within the current treatment paradigm for HER2-positive metastatic breast cancer.

這也進一步驗證了我們在 ASPEN-6 試驗中，Evo 與 HER2 陽性胃癌所觀察到的結果。我們也很高興今天邀請到華盛頓大學 Fred Hutch 癌症中心的 Sara Hurvitz 醫師一同參與，她是轉移性乳癌領域廣受認可的專家。她將詳細介紹 ESMO 乳癌會議的數據，並分享她對 evorpacept 在目前 HER2 陽性轉移性乳癌治療典範中具重大潛力的看法。

Our CMO, Barb Klencke, will then recap our findings to date with Evo and HER2-positive cancers across now two different independent trials and indications, showing that patients with high CD47 expression derive the greatest benefit across all key efficacy markers, including overall response rates, duration of response and PFS versus those with low expression.

接著，我們的首席醫學長（CMO）Barb Klencke 將回顧迄今為止 Evo 在 HER2 陽性癌症上的研究發現——目前已涵蓋兩項彼此獨立的試驗與適應症——顯示 CD47 高表現的患者在所有關鍵療效指標上獲益最大，包括總反應率、反應持續時間以及無惡化存活期（PFS），相較於 CD47 低表現者更為明顯。

These results support our targeted oncology approach with Evo, notably our ongoing ASPEN-09 breast cancer Phase II trial. Barb will then provide an update from our ongoing Phase I trial with our novel EGFR-targeted ADC, ALX2004, which also continues to track to plan, and we are enthusiastic about its potential to also change care in EGFR-expressing cancers.

這些結果支持我們以 Evo 推動的精準腫瘤學策略，尤其是我們正在進行的 ASPEN-09 乳癌第二期試驗。接著 Barb 也將就我們新型 EGFR 標靶 ADC（抗體藥物複合體）ALX2004 的第一期試驗提供最新進度；該試驗持續按計畫推進，我們也對其在 EGFR 表現型癌症中改變照護模式的潛力感到振奮。

So on slide 4, we continue to advance both our programs, Evo and ALX2004 and are pleased with the progress on both fronts over the course of Q1 and remain well positioned to report on significant data readouts from these programs in the coming 12 to 18 months. On the Evo front, CD47, as you know, is incredibly important in oncology and has been a very difficult target to crack, yet it plays a fundamental role in tumor evasion and resistance.

因此在投影片第 4 頁，我們持續推進兩項計畫——Evo 與 ALX2004——並對第一季期間兩方面的進展感到滿意；我們也維持良好態勢，預期在未來 12 至 18 個月內，將可就這些計畫的重要數據讀出進行報告。在 Evo 方面，大家都知道 CD47 在腫瘤學中極其重要，且一直是非常難以攻克的標的，但它在腫瘤免疫逃逸與抗藥性上扮演根本性的角色。

We've been happy to see Evo's differentiated approach to this target further validated in the clinic over now five different data sets, including randomized data. Further, the new data from this week's ESMO meeting and over the last year support CD47 as a strong and predictive biomarker. These new findings further support the drug is working as designed and also enables a targeted strategy, which allows us to focus on the patients who will benefit most.

我們很高興看到 Evo 對此標的的差異化策略，至今已在臨床上透過五個不同資料集（包含隨機分派數據）獲得進一步驗證。此外，本週 ESMO 會議的新數據以及過去一年的結果，都支持 CD47 是一個強而有力且具預測性的生物標誌。這些新發現進一步支持該藥物如設計般發揮作用，並使我們能採取精準策略，聚焦於最可能受益的患者。

On ALX2004, as you know, it is a highly differentiated EGFR-targeted ADC, which was developed in-house by ALX and has the potential to be a first-in-class EGFR-targeted ADC. EGFR has also been a difficult target for ADCs historically, and ALX2004 was designed to address this with a novel epitope and linker payload construct.

至於 ALX2004，如各位所知，它是一款高度差異化的 EGFR 標靶 ADC，由 ALX 內部自行研發，並有潛力成為同類首創（first-in-class）的 EGFR 標靶 ADC。歷史上 EGFR 也是 ADC 開發中相當棘手的標的，而 ALX2004 透過新穎的表位（epitope）以及連接子-載荷（linker payload）結構設計，旨在解決這些挑戰。

We have been pleased to see the strong preclinical data to date translate to the clinic and with the continued strong progress in dose escalation, where we have been able to further increase dose. Overall, both programs remain on track and well positioned. Now on slide 4, Q1 was a quarter of continued good execution and additional positive data as well as completion of key hires and a strong financing.

我們很高興看到迄今強勁的臨床前數據已成功轉譯到臨床，且在劑量遞增方面持續取得良好進展，我們也得以進一步提高劑量。整體而言，兩項計畫皆維持在正軌上，且具備良好推進條件。回到投影片第 4 頁，第一季我們持續良好執行，取得更多正面數據，同時完成關鍵人才招募並完成一筆強勁的融資。

As you'll hear more about shortly, this week's data validate again the power of CD47 in a late-stage patient population. Here, we observed that all patients who were confirmed HER2-positive and CD47 high achieved a response, including one complete response. We also yet again saw the durability that one hopes to see with an IO mechanism with a median duration of response of 20 months and a median PFS of 22 months, which is clearly far improved over the benchmarks.

如各位稍後將聽到的，本週的數據再次驗證 CD47 在晚期患者族群中的強大作用。在此我們觀察到：所有經確認為 HER2 陽性且 CD47 高表現的患者皆達到反應，其中包含 1 例完全反應。我們也再次看到人們對免疫腫瘤（IO）機制所期待的持久性：反應持續時間中位數為 20 個月、PFS 中位數為 22 個月，顯然大幅優於既有基準。

While the focus for today will be on this new data set with Evo, ALX2004 is also progressing through dose escalation very well and remains on track for initial safety readout in the second half of this year. We remain as excited here about its potential as we do with Evo. Further, the financing from February, which was anchored by very strong investors, further strengthens the balance sheet and enables us to execute through these important data milestones.

雖然今天的重點將放在 Evo 的這組新數據上，ALX2004 也在劑量遞增階段進展順利，並仍按計畫於今年下半年進行初步安全性讀出。我們對其潛力的興奮程度不亞於 Evo。此外，2 月份的融資由實力雄厚的投資人領投，進一步強化資產負債表，並使我們能夠推進並完成這些重要數據里程碑。

And last but certainly not least, we added Jeff Knight, who is now our Chief Development and Chief Operating Officer, which really further strengthens our leadership team. Jeff, as you may know, is one of the best operators in biotech in terms of building companies at our stage through the next phase, including commercialization.

最後但同樣重要的是，我們延攬 Jeff Knight 加入，他現任我們的首席開發長兼首席營運長，這確實進一步強化了我們的領導團隊。如各位所知，Jeff 在生技產業中是頂尖的營運操盤手之一，擅長協助我們這個階段的公司邁向下一階段，包括商業化。

On slide 6, briefly, this just highlights the execution, clinical development progress and time lines, which remain on track for both programs. Our evorpacept Phase II breast trial continues to progress well with strong enrollment globally and increasing site enthusiasm. Overall, clinical time lines remain on track as we're expected to read out 80 patients mid next year.

在投影片第 6 頁，簡要說明我們的執行成果、臨床開發進展與時程，兩項計畫皆維持按計畫推進。我們的 evorpacept 乳癌第二期試驗持續進展良好，全球收案強勁，且各研究中心的投入熱度持續提升。整體臨床時程仍在正軌上，預計明年年中將讀出 80 名患者的數據。

ALX2004, as I mentioned, is also progressing well with enrollment and dose escalation ramping and are on track there for an initial safety readout in the second half of this year. Our goal and vision for both of these programs also remains unchanged as we aim to have both programs ready for registrational studies by end of next year.

如我所提，ALX2004 也在收案與劑量遞增加速推進方面進展良好，並按計畫於今年下半年提供初步安全性讀出。我們對這兩項計畫的目標與願景也維持不變：力求在明年年底前，讓兩項計畫都具備進入註冊性試驗的準備。

On slide 7 and my last slide, here is also a snapshot of our clinical pipeline. As you know, we're advancing 2 novel cancer treatments with key near-term catalysts. And again, ASPEN-Breast is on track. And we continue to also be encouraged by our ongoing study with our partner, Sanofi, testing Evo in multiple myeloma. Our two studies in HER2-positive cancers have now been completed as we'll focus on today and ALX2004 also remains on track.

在投影片第 7 頁，也是我最後一張投影片，這裡提供我們臨床產品線的概覽。如各位所知，我們正推進兩項新型癌症治療，且短期內有多個關鍵催化劑。同樣地，ASPEN-Breast 仍按計畫推進。我們也持續受到與合作夥伴賽諾菲（Sanofi）進行的研究所鼓舞，該研究正在多發性骨髓瘤中測試 Evo。我們在 HER2 陽性癌症的兩項研究現已完成——這也是我們今天將聚焦的內容——而 ALX2004 也仍按計畫推進。

I'd like to now turn the call to Barb, who will provide a quick reminder of our MOA, which is very important as we're clearly seeing it translate to the clinic, and we'll then turn the call over to Dr. Hurvitz to review the new data. Barb?

接下來我想把電話會議交給 Barb，她將快速提醒各位我們的作用機轉（MOA）；這點非常重要，因為我們顯然正看到其在臨床上的轉譯效果。之後我們將把會議交給 Hurvitz 醫師來回顧新數據。Barb？

Thank you, Jason. These next few slides describe evorpacept's mechanism of action. What's so compelling to me is that the mechanism of action is entirely consistent with what we see in the clinical trials. So let me just go through this. Cancer cells commonly upregulate CD47 expression to evade immune detection. Evorpacept blocks the CD47 signaling, but it does so without an active Fc domain.

謝謝你，Jason。接下來幾張投影片將說明 evorpacept 的作用機轉。我認為最引人注目的是：其作用機轉與我們在臨床試驗中所看到的結果完全一致。我簡單帶各位看一下。癌細胞通常會上調 CD47 的表現，以躲避免疫系統的偵測。Evorpacept 會阻斷 CD47 訊號傳導，但其方式是不具活性 Fc 結構域。

So evorpacept by itself does not engage the phagocytic activity of a macrophage. We need to combine evorpacept with an anticancer antibody. And then the combination together strongly augments the ADCP activity of the antibody. And that's likely what results in the efficacy that we see in the studies that we'll talk about today.

因此，evorpacept 單獨使用並不會啟動巨噬細胞的吞噬活性。我們需要將 evorpacept 與抗癌抗體合併使用。然後，這種合併治療會強力增強該抗體的 ADCP 活性。而這很可能就是我們在今天將要討論的研究中所看到療效的原因。

Essentially, the antibody stimulates the eat-me signal, and the evorpacept inhibits the don't eat me signal. Therefore, the combinations of evorpacept with an antibody are selectively enhancing or augmenting macrophage phagocytosis of cells that express HER2, for example, in the case of a HER2-targeted antibody while also blocking the don't eat me signal.

本質上，抗體會刺激「吃我」訊號，而 evorpacept 會抑制「不要吃我」訊號。因此，evorpacept 與抗體的合併治療會選擇性地增強或提高巨噬細胞對表達 HER2 的細胞之吞噬作用——例如在使用 HER2 標靶抗體的情況下——同時也阻斷「不要吃我」訊號。

On the next slide, we see how this mechanism of action translates into safety. Our clinical safety database is now more than 800 evorpacept-treated patients. And it also -- the clinical safety data is also entirely consistent with this mechanism of action that we show here. Evorpacept was designed again without an active Fc domain. That's shown on the right side of the slide.

在下一張投影片中，我們可以看到這種作用機轉如何轉化為安全性。我們的臨床安全性資料庫目前已包含超過 800 名接受 evorpacept 治療的患者。而且——這些臨床安全性資料也完全與我們在此所展示的作用機轉一致。Evorpacept 的設計再次強調不含活性 Fc 結構域。這點在投影片右側有所呈現。

So when we block the don't eat me signal on normal healthy cells, such as red blood cells, there is no macrophage activation, and we avoid on-target toxicities. This is really fundamentally different than what's been tried in the past by conventional CD47 inhibitors, which have essentially failed in the clinic. They attempted to use CD47 as a tumor-associated antigen with both an active Fc domain to activate macrophage at the same time of blocking CD47.

因此，當我們在正常健康細胞（例如紅血球）上阻斷「不要吃我」訊號時，並不會造成巨噬細胞活化，從而避免標的相關毒性（on-target toxicities）。這在根本上不同於過去傳統 CD47 抑制劑所嘗試的方法，而那些方法在臨床上基本上已告失敗。它們試圖將 CD47 作為腫瘤相關抗原，並同時使用具有活性 Fc 結構域來活化巨噬細胞，且在阻斷 CD47 的同時進行。

That ended up being an indiscriminate approach because CD47 is so widely expressed on healthy cells, especially hematologic cells in particular. And that led to the potential for significant on-target toxicity. So with that description of evorpacept, its mechanism of action and its differentiation, let me now turn the conversation over to Dr. Sara Hurvitz.

但那最終成為一種不加區分的策略，因為 CD47 在健康細胞上表達非常廣泛，尤其是在血液系統細胞上更為明顯。這也導致可能出現顯著的標的相關毒性。在以上對 evorpacept、其作用機轉及差異化的說明之後，接下來我把談話交給 Sara Hurvitz 醫師。

On slide 12, you can see her background here. She is a steering committee member for our ASPEN-09 Phase II study of evorpacept in HER2-positive breast cancer patients. She was an investigator on the evorpacept and zanidatamab trial that we'll discuss today. And she's a Senior Vice President, a Professor of Clinical Research and the Director of the Clinical Research Division at the Fred Hutch Cancer Center at the University of Washington in Seattle, where she's also the Head of the Division of Hematology and Oncology and the Smith Family and Dow Chair of Women's Health. She's an expert in the management of breast cancer and in the development of novel targeted therapies for breast cancer. Sara?

在第 12 張投影片中，您可以看到她的背景介紹。她是我們 ASPEN-09 第二期研究（針對 HER2 陽性乳癌患者使用 evorpacept）的指導委員會成員。她也是我們今天將討論之 evorpacept 與 zanidatamab 試驗的研究者。此外，她是華盛頓大學西雅圖 Fred Hutch 癌症中心臨床研究部門的資深副總裁、臨床研究教授暨臨床研究部門主任；同時也是血液腫瘤科部門主管，以及 Smith Family and Dow 女性健康講座教授。她是乳癌治療管理與乳癌新型標靶療法開發方面的專家。Sara？

Thanks, Barb. I'm really excited to be here today. There have been remarkable changes in the management of HER2-positive breast cancer, especially since 2020, with new agents like trastuzumab, deruxtecan and tucatinib demonstrating benefits in pretreated disease. And with the results of DESTINY-Breast09 showing benefits with T-DXd in combination with pertuzumab, we have a new standard of care according to our NCCN guidelines as of this February.

謝謝你，Barb。我今天能在這裡感到非常興奮。HER2 陽性乳癌的治療管理出現了顯著變化，尤其自 2020 年以來，像 trastuzumab deruxtecan 與 tucatinib 等新藥在既往治療過的疾病中展現了效益。而隨著 DESTINY-Breast09 顯示 T-DXd 與 pertuzumab 合併治療帶來益處，根據我們 NCCN 指南在今年 2 月更新後，已形成新的標準治療。

What we don't know is how we should be treating patients after they've received ENHERTU. This remains an area of unmet need. On slide 14, you can see this graph showing the outcomes that we have from patients who've received prior ENHERTU treatment with a median progression-free survival of only 4.1 months. What we don't have are randomized prospective data telling us as clinicians how we should manage patients after T-DXd, but observational and retrospective data sets are fairly consistent, showing that PFS rates of under six months is what patients experience post T-DXd.

我們尚不清楚的是：患者在接受 ENHERTU 之後，應該如何治療。這仍是一個未被滿足的醫療需求領域。在第 14 張投影片中，您可以看到這張圖表顯示既往接受 ENHERTU 治療患者的結果，其中位無惡化存活期（PFS）僅 4.1 個月。我們缺乏隨機、前瞻性資料來告訴臨床醫師在 T-DXd 之後應如何管理患者，但觀察性與回溯性資料集相當一致，顯示患者在 T-DXd 之後的 PFS 多低於 6 個月。

On the next slide, on slide 15, you can see the list of HER2-directed therapies that we have approved and in late-stage development on the left side. These include HER2-targeted antibodies and bispecifics, HER2-targeted antibody drug conjugates and HER2-targeted tyrosine kinase inhibitors as well. What we don't have are immuno-oncology therapies approved or in late-stage development outside of evorpacept.

在下一張投影片、第 15 張投影片中，您可以在左側看到目前已核准以及處於後期開發階段的 HER2 導向治療清單。其中包括 HER2 標靶抗體與雙特異性抗體、HER2 標靶抗體藥物複合體（ADC），以及 HER2 標靶酪胺酸激酶抑制劑。但我們目前沒有在 evorpacept 之外、已核准或處於後期開發階段的免疫腫瘤（immuno-oncology）療法。

And so this remains an area that's very exciting to see developed now. On slide 16, you can see the range of CD47 expression in normal cells versus tumor cells. As explained before, CD47 is expressed on all cell types and is a marker of cells and cancer cells can take advantage of this by overexpressing CD47, allowing them to hide from the immune system.

因此，看到這個領域現在開始發展，仍然令人非常振奮。在第 16 張投影片中，您可以看到正常細胞與腫瘤細胞之間 CD47 表達的範圍。如先前所述，CD47 在所有細胞類型上都有表達，是細胞的標記；而癌細胞可藉由過度表達 CD47 來加以利用，使其得以躲避免疫系統。

Focusing on the left there, you can see highlighted in blue, breast cancer cell lines, which actually do have higher expression of CD47 in tumors compared to normal, which is highlighted in black. On slide 17, you can see a meta-analysis of 38 cohorts across 17 publications, which included over 7,000 patients, demonstrating fairly consistently that CD47 overexpression was correlated with shorter survival in patients with cancer.

聚焦在左側，您可以看到以藍色標示的乳癌細胞株；相較於以黑色標示的正常細胞，腫瘤中的 CD47 表達確實更高。在第 17 張投影片中，您可以看到一項涵蓋 17 篇出版物、38 個隊列的統合分析（meta-analysis），納入超過 7,000 名患者，相當一致地顯示 CD47 過度表達與癌症患者較短的存活期相關。

So it's a negative prognostic biomarker. On slide 18, there are data here relating to CD47 expression in breast cancer, in particular, in HER2-positive breast cancer. On the left, you can see that CD47 expression is higher on HER2-positive breast cancer cells versus HER2-negative on the right. High expression is denoted in the dark blue, moderate expression in green and low expression in blue.

因此，它是一個不良預後的生物標記。在第 18 張投影片中，這裡有與乳癌中 CD47 表達相關的資料，特別是 HER2 陽性乳癌。在左側，您可以看到 HER2 陽性乳癌細胞的 CD47 表達高於右側的 HER2 陰性。高表達以深藍色表示，中度表達以綠色表示，低表達以藍色表示。

So HER2-positive breast cancer cells appear to have a lot more CD47 expressed than HER2-negative breast cancer cells. And in fact, if you look on the right side, you can see that CD47 high cells are more common in recurrent HER2-positive breast cancer shown on the left side compared to primary or initially diagnosed breast cancer.

因此，HER2 陽性乳癌細胞似乎表達了更多的 CD47，較 HER2 陰性乳癌細胞為高。事實上，如果您看右側，會看到 CD47 高表達細胞在復發性 HER2 陽性乳癌中更常見（左側所示），相較於原發或初次診斷的乳癌。

And so these data provide strong rationale for us to be evaluating evorpacept in HER2-positive recurrent or metastatic pretreated disease. On slide 19, you can see some elegant data demonstrating that T-DXd treatment may actually upregulate expression of CD47, again, providing strong rationale to treat HER2-positive recurrent T-DXd pretreated breast cancer with evorpacept.

因此，這些資料為我們評估 evorpacept 用於 HER2 陽性復發或轉移、且已接受過治療的疾病提供了強而有力的理據。在第 19 張投影片中，您可以看到一些精緻的資料顯示 T-DXd 治療可能實際上會上調 CD47 的表達，再次提供強而有力的理據，支持以 evorpacept 治療 HER2 陽性復發、且已接受 T-DXd 治療的乳癌。

On slide 20, you can see the title slide for the data presented recently at ESMO breast. This is an exploratory biomarker analysis from our Phase Ib/II trial of zanidatamab, a HER2-targeted bispecific in combination with evorpacept in patients with HER2-positive metastatic disease. Slide 21 gives you an overview of the study design.

在第 20 張投影片中，您可以看到最近在 ESMO breast 發表之資料的標題頁。這是一項探索性生物標記分析，來自我們的 Ib/II 期試驗：在 HER2 陽性轉移性疾病患者中，評估 HER2 標靶雙特異性抗體 zanidatamab 與 evorpacept 的合併治療。第 21 張投影片提供研究設計的概覽。

This is a Phase Ib/II study, and we presented the safety dose escalation cohort data from three patients with HER2-positive breast cancer enrolled and data from Cohort 1, where 21 patients with HER2-positive breast cancer were enrolled who had received at least three prior regimens. The exploratory biomarker analyses focused on these 24 patients, and it's notable that all of the HER2-positive cohort received prior T-DXd and a median of five prior lines of HER2-targeted therapies.

這是一項 Ib/II 期研究；我們呈現了劑量遞增安全性隊列中 3 名納入的 HER2 陽性乳癌患者資料，以及第 1 隊列的資料：該隊列納入 21 名 HER2 陽性乳癌患者，且皆至少接受過 3 種既往治療方案。探索性生物標記分析聚焦於這 24 名患者；值得注意的是，所有 HER2 陽性隊列患者皆曾接受 T-DXd，且既往 HER2 標靶治療的中位線數為 5 線。

This is extremely heavily pretreated disease. The patients were allowed to enter the study based on prior local HER2 testing of their archival tissue. However, fresh baseline biopsies were obtained in most patients and tested retrospectively for HER2 status by central assessment. And we will be reviewing outcome results based on the central assessment as well as the intent-to-treat population.

這是極度重度預先治療的疾病。患者可依其既往對存檔組織所做的當地 HER2 檢測結果而納入本研究。然而，多數患者取得了新鮮的基線活檢，並由中央評估回溯性檢測 HER2 狀態。我們將根據中央評估結果以及意向治療（ITT）族群來回顧療效結果。

In addition, patients' tumors were tested for CD47 expression on the fresh baseline tumor biopsies or on archival tissue if fresh biopsies were not available. Patients were treated with zanidatamab at 1,200 milligrams for those patients weighing less than 70 kilograms and at 1,600 milligrams for patients 70 kilograms or greater.

此外，患者腫瘤的 CD47 表現是在新鮮基線腫瘤活檢上檢測；若無法取得新鮮活檢，則使用存檔組織檢測。zanidatamab 的給藥為：體重小於 70 公斤者 1,200 毫克；體重達 70 公斤或以上者 1,600 毫克。

The evorpacept was given at 20 mg per kg for these three patients enrolled in the Ia or at 30 mg per kg IV every two weeks for the rest of the patients. Going on to slide 22, we're jumping to the efficacy outcome data. What you can see here are the confirmed objective response rate on the top row based on all 24 patients, which is 33%.

evorpacept 的給藥為：納入 Ia 的這三位患者以每公斤 20 mg 給藥；其餘患者則以每公斤 30 mg 靜脈注射（IV），每兩週一次。接著到第 22 張投影片，我們跳到療效結果資料。您在此看到的是以全部 24 位患者為基礎、上排所示的經確認客觀反應率（ORR），為 33%。

I find personally these data to be quite impressive in patients who've received a median of five prior lines of therapy, including T-DXd. If you go down to the duration of response, those patients who experienced a response had a duration of response of 20 months and a median progression-free survival of 3.6 months. The next column shows the outcomes for the 6 -- excuse me, for the 10 patients who had centrally confirmed HER2-positive breast cancer, where the objective response rate was now 60%.

就我個人而言，這些資料在既往治療中位數達 5 線（包含 T-DXd）的患者中相當令人印象深刻。若看反應持續時間（DOR），出現反應的患者其 DOR 為 20 個月，而中位無惡化存活期（PFS）為 3.6 個月。下一欄顯示的是 10 位（抱歉，不是 6 位）中央確認為 HER2 陽性乳癌患者的結果，此時客觀反應率提升至 60%。

The duration of response was 20.2 months and the median PFS was 8.3 months. These data, I think, are impressive as we reflect back on the fact that our retrospective and observational data suggests that patients pretreated with T-DXd have a median PFS of less than six months. So I find these data to be quite compelling and exciting.

反應持續時間為 20.2 個月，中位 PFS 為 8.3 個月。當我們回顧回溯性與觀察性資料所顯示：接受過 T-DXd 預先治療的患者其中位 PFS 少於 6 個月時，我認為這些資料相當亮眼。因此我覺得這些資料非常有說服力，也令人振奮。

Those patients who did not have centrally confirmed HER2-positive disease had a lower objective response rate of 14%. On slide 23, we can now see breakdown based on the tumor CD47 expression levels. Using a cutoff of at least 20% for CD47 expression, there are five patients who had both centrally confirmed HER2-positive disease and CD47 positive or greater than or equal to 20% expression.

未被中央確認為 HER2 陽性疾病的患者，其客觀反應率較低，為 14%。在第 23 張投影片，我們可以看到依腫瘤 CD47 表現量分層的結果。以 CD47 表現至少 20% 作為切點，有 5 位患者同時具備中央確認的 HER2 陽性疾病，且 CD47 為陽性（或表現量 ≥20%）。

All patients had an objective response in this cohort of 5 patients with a median DOR of 20.2 months. However, those patients whose CD47 expression was less than 20%, that's four patients, only one had an objective response. So this is beginning to give us data that CD47 expression level may be a marker to help us select patients particularly responsive to this targeted therapy.

在這 5 位患者的隊列中，所有患者皆達到客觀反應，其中位 DOR 為 20.2 個月。然而，CD47 表現低於 20% 的患者共有 4 位，僅 1 位出現客觀反應。因此，這開始提供我們一些資料：CD47 表現量可能是一個標記，有助於我們篩選對此標靶治療特別有反應的患者。

On slide 24, you can see a Kaplan-Meier curve for progression-free survival based on CD47 expression levels. So the progression-free survival with the CD47 expression level of at least 20%, you can see the PFS is 22 months, for those patients less than 20% of the PFS is 3.4 months. Again, although these numbers are very small, we're talking about nine patients total.

在第 24 張投影片，您可以看到依 CD47 表現量分層的無惡化存活期 Kaplan-Meier 曲線。CD47 表現量至少 20% 的患者，其 PFS 為 22 個月；而低於 20% 的患者，其 PFS 為 3.4 個月。再次強調，雖然這些數字非常小，我們總共只談到 9 位患者。

The data are quite interesting, and I'm excited to see them hopefully confirmed in the larger study. On slide 25 are our conclusions for this exploratory analysis of our Phase Ib/II study. Evorpacept and zanidatamab showed promising antitumor activity in patients with heavily pretreated HER2-positive metastatic breast cancer, median of five prior lines of therapy, all of whom received prior T-DXd. Greater antitumor activity was seen in patients with centrally confirmed HER2-positive disease.

這些資料相當有趣，我也期待能在更大型的研究中獲得驗證。第 25 張投影片是我們對此第 Ib/II 期研究探索性分析的結論。在重度預先治療的 HER2 陽性轉移性乳癌患者中（既往治療中位數 5 線，且皆曾接受 T-DXd），evorpacept 與 zanidatamab 顯示出具前景的抗腫瘤活性。在中央確認為 HER2 陽性的患者中，觀察到更高的抗腫瘤活性。

Durable responses were seen in this patient population and seem to be largely observed in patients with higher CD47 expression, supporting a CD47dependent HER2-driven biology that resulted in this prolonged progression-free survival. It's notable that most patients with centrally confirmed HER2-positive disease remained HER2 amplified at progression with T-DXd, supporting the continued use of HER2-targeted therapies. And so a biomarker-driven approach incorporating CD47 may optimize patient selection for this combination regimen and warrants further study.

在此患者族群中可見持久反應，且似乎主要出現在 CD47 表現較高的患者，支持一種 CD47 依賴、HER2 驅動的生物學機制，進而帶來較長的無惡化存活期。值得注意的是，多數中央確認為 HER2 陽性的患者在 T-DXd 治療惡化時仍維持 HER2 擴增，支持持續使用 HER2 標靶治療。因此，納入 CD47 的生物標記驅動策略可能可最佳化此合併療法的患者選擇，並值得進一步研究。

So with that, I will turn it back over to Barb.

那麼，我把時間交回給 Barb。

Thank you, Sara for that excellent presentation. As we've seen, all of the patients who were centrally assessed as HER2-positive and who overexpressed CD47 in their cancer cells achieved confirmed response to the combination of evorpacept plus zanidatamab. What's new on slide 27 in the table on the right side of this slide are the individual CD47 expression levels and the confirmed response assessments for each of the 10 patients with centrally assessed HER2-positive disease.

謝謝你，Sara，帶來這場精彩的報告。如我們所見，所有經中央評估為 HER2 陽性且其癌細胞 CD47 過度表現的患者，在 evorpacept 加上 zanidatamab 的合併治療下皆達到經確認的反應。第 27 張投影片右側表格的新內容，是 10 位中央評估為 HER2 陽性患者各自的 CD47 表現量，以及每位患者的經確認反應評估。

An IHC assay was used to quantify the total membrane staining for CD47. A positive result was defined retrospectively as a score of 20% or higher, which we observed in the patients shown in the top five rows highlighted with deep blue. All five of these patients with CD47 expression responded, including one patient with a complete response.

使用 IHC（免疫組織化學）檢測來量化 CD47 的總膜染色。回溯性地將陽性結果定義為分數達 20% 或以上；我們在上方五列（以深藍色標示）的患者中觀察到此結果。這 5 位 CD47 表現的患者皆有反應，其中包含 1 位患者達到完全反應。

That patient happened to be the only patient from the dose escalation cohort that was centrally assessed as HER2-positive. There was no evidence of CD47 overexpression in the four patients highlighted in light gray, one of whom responded to the evorpacept and zanidatamab combination. And then in the last row in this table is a patient who was unevaluable for either response or CD47 expression level.

該患者剛好是劑量遞增隊列中唯一一位經中央評估為 HER2 陽性的患者。在以淺灰色標示的 4 位患者中未見 CD47 過度表現，其中 1 位對 evorpacept 與 zanidatamab 的合併治療有反應。而此表最後一列是一位在反應或 CD47 表現量方面皆無法評估的患者。

On slide 28, I want to highlight the consistency that we see between the results of the evorpacept, zanidatamab trial in HER2-positive breast cancer patients and in the previously reported HER2-positive gastric study. On the top half of the slide, you'll see the data that we've just reviewed. This includes a 33% response rate in the 24 patients enrolled based on archival HER2 status, the 60% response rate in the 10 patients centrally assessed as HER2-positive and the 100% response rate in the five patients who were also CD47 overexpressing.

在第 28 張投影片，我想強調我們在 HER2 陽性乳癌患者的 evorpacept、zanidatamab 試驗結果，與先前報告的 HER2 陽性胃癌研究之間所見的一致性。在投影片上半部，您會看到我們剛剛回顧的資料。其中包括：依存檔 HER2 狀態納入的 24 位患者反應率 33%；中央評估為 HER2 陽性的 10 位患者反應率 60%；以及同時 CD47 過度表現的 5 位患者反應率 100%。

On the bottom half of this slide, you see the data from ASPEN-06. This is a randomized Phase II study of evorpacept, trastuzumab, paclitaxel and ramucirumab versus the TRP regimen alone. Here, you see the response rate climb as we look across the slide at the same subset. In the ITT, the response rates in patients randomized to the evorpacept arm was 41%. Response rate was over 49% in the patients that retained HER2-positive disease, and it was 65% in patients whose tumors also expressed CD47.

在投影片下半部，您會看到 ASPEN-06 的資料。這是一項隨機分派的第 II 期研究，比較 evorpacept、trastuzumab、paclitaxel 與 ramucirumab 的合併治療，對照僅 TRP 方案。在此，當我們以相同子集橫向比較時，可看到反應率逐步上升。在 ITT 族群中，隨機分派至 evorpacept 組的患者反應率為 41%。在仍維持 HER2 陽性疾病的患者中，反應率超過 49%；而在腫瘤亦表現 CD47 的患者中，反應率為 65%。

And recall, this was a large Phase II study of 127 patients. As you see, the data trends here are consistent across these two independent trials of evorpacept when combined with a HER2-targeted antibody. On slide 29, I'm again showing the results of the Evo-Zani study on the top and the ASPEN-06 HER2-positive gastric study on the bottom.

請回想，這是一項大型第 II 期研究，共 127 位患者。如您所見，當 evorpacept 與 HER2 標靶抗體合併使用時，這兩項獨立試驗的資料趨勢一致。在第 29 張投影片，我再次呈現上方的 Evo-Zani 研究結果，以及下方的 ASPEN-06 HER2 陽性胃癌研究結果。

The graph -- these graphs show the duration of response in the subset of patients who were HER2-positive and CD47 overexpressing in the two independent studies. The duration of response was remarkable in both settings at 20.2 months and 25.5 months, respectively. On slide 30, the same consistency across the two independent studies as seen with the PFS results in the subset of HER2-positive CD47 high patients.

這張圖——這些圖表顯示在兩項獨立研究中，HER2 陽性且 CD47 過度表現之患者子集的反應持續時間。在兩種情境下的反應持續時間都相當顯著，分別為 20.2 個月與 25.5 個月。在第 30 張投影片中，可看到與 PFS 結果相同的趨勢：在 HER2 陽性、CD47 高表現患者子集中，兩項獨立研究之間呈現一致性。

Both studies show a remarkably long PFS, especially in light of the later line settings for both indications. On the left, we see the median PFS for these patients in the evorpacept-zanidatamab study of 22.1 months, while the median PFS for those without CD47 expression was only 3.4 months. And then in the gastric study, shown on the right, the median PFS was 18.4 months for the patients in the evorpacept arm and the hazard ratio in this subset in the randomized trial was 0.39.

兩項研究都顯示出顯著延長的 PFS，尤其考量到兩個適應症皆屬較後線治療情境。左側可見，在 evorpacept-zanidatamab 研究中，這些患者的中位數 PFS 為 22.1 個月，而未表現 CD47 的患者其中位數 PFS 僅為 3.4 個月。而在右側所示的胃癌研究中，evorpacept 組患者的中位數 PFS 為 18.4 個月，且在隨機試驗的此子集中，風險比為 0.39。

So these data are really why we're so excited about moving forward with the development of evorpacept in HER2-positive breast cancer. slide 31 shows our ongoing ASPEN-09 study in the HER2-positive breast cancer setting. Like the zanidatamab-evorpacept study population, all of these patients will have had to have had prior ENHERTU. This is going to -- this is a single-arm study that will enroll up to 120 patients and has a primary endpoint of response rate in the subset of patients who overexpress CD47.

因此，這些數據正是我們對於推進 evorpacept 在 HER2 陽性乳癌之開發感到非常振奮的原因。第 31 張投影片顯示我們正在進行的 ASPEN-09 研究，針對 HER2 陽性乳癌情境。如同 zanidatamab-evorpacept 研究族群，所有這些患者都必須曾接受過 ENHERTU 治療。這將會——這是一項單臂研究，最多將納入 120 名患者，主要終點為 CD47 過度表現患者子集的反應率。

We're making very good progress with enrollment, and we're very much on track to achieve our stated milestone of having interim top line data from approximately 80 patients by the middle of 2027. On slide 32, we show the market opportunity. Ultimately, our aim, of course, is to bring this drug to market. We estimate that there are approximately 20,000 addressable patients who are HER2-positive and overexpress CD47, representing a $2 billion to $4 billion market opportunity in the United States, the 5 major European markets and Japan.

我們在收案方面進展非常順利，也完全按計畫達成我們所宣示的里程碑：於 2027 年年中以前，取得約 80 名患者的期中頂線（top line）數據。在第 32 張投影片中，我們展示市場機會。當然，我們的最終目標是將此藥物推向市場。我們估計約有 20,000 名可觸及患者為 HER2 陽性且 CD47 過度表現，代表在美國、歐洲五大主要市場及日本合計約 20 億至 40 億美元的市場機會。

I'm now going to turn for the last few minutes of this talk to our second molecule. slide 34 shows ALX2004, our EGFR antibody drug conjugate. This is actually a very unique molecule. It was designed by protein engineers and cancer biologists within ALX. EGFR is obviously a very validated target, but it's been very difficult to target EGFR in the past with an antibody drug conjugate.

接下來我將用本次演講最後幾分鐘談談我們的第二個分子。第 34 張投影片顯示 ALX2004，我們的 EGFR 抗體藥物複合體（ADC）。這其實是一個非常獨特的分子。它由 ALX 內部的蛋白質工程師與癌症生物學家所設計。EGFR 顯然是一個高度驗證的標的，但過去以抗體藥物複合體來鎖定 EGFR 一直非常困難。

We selected amituzumab-derived EGFR antibody to minimize off-tumor skin toxicity and to maximize the therapeutic window. Also, the epitope is distinct from that of FDA-approved EGFR antibodies, minimizing the likelihood of resistance to prior EGFR antibody treatment. The proprietary linker allows for lysosomal cleavage of the linker payload like other deruxtecan ADCs, but the stability of the linker antibody has been enhanced to minimize systemic payload release.

我們選用源自 amituzumab 的 EGFR 抗體，以降低腫瘤外皮膚毒性並最大化治療窗。此外，其表位與 FDA 核准的 EGFR 抗體不同，可降低對既往 EGFR 抗體治療產生抗藥性的可能性。專有連接子可在溶酶體中切割並釋放連接子-載荷，類似其他 deruxtecan 類 ADC，但我們也提升了連接子-抗體的穩定性，以將全身性載荷釋放降至最低。

The molecule also contains a proprietary TOPO1 inhibitor payload. It has an antibody drug ratio of 8, and the payload has similar direct cytotoxic potency, but it has enhanced bystander activity compared to deruxtecan. On slide 35, we show the Phase I design. This is an ongoing study, and the study is designed for dose escalation, dose exploration and expansion cohorts.

該分子亦包含專有的 TOPO1 抑制劑載荷。其抗體藥物比（DAR）為 8，載荷具有相近的直接細胞毒性效力，但相較於 deruxtecan 具有更強的旁觀者效應（bystander activity）。在第 35 張投影片中，我們展示第一期試驗設計。這是一項正在進行的研究，設計包含劑量遞增、劑量探索以及擴增隊列。

The study is limited to patients who have lung cancer, head and neck cancer, colorectal cancer or esophageal cancer as EGFR expression is higher in these indications. And in this study, we're also making very good progress with enrollment. We are certainly on track to achieve our stated milestone of reporting initial safety data within the second half of 2026.

本研究僅納入肺癌、頭頸癌、大腸直腸癌或食道癌患者，因為在這些適應症中 EGFR 表現較高。在這項研究中，我們的收案進展也非常良好。我們確實按計畫可在 2026 年下半年報告初步安全性數據，以達成既定里程碑。

We previously publicly released information that we began dose escalation at 1 milligram. We then said we escalated to 2 milligrams. And then we announced that we had escalated to 4 milligram per kilogram dose cohort. But as we advance the enrollment and dose escalation in this trial, we are now shifting from providing granular updates to reporting initial safety data in the second half of 2026.

我們先前已公開發布資訊，表示我們從 1 毫克開始進行劑量遞增。之後我們表示已遞增至 2 毫克。接著我們宣布已遞增至 4 毫克/公斤的劑量隊列。但隨著本試驗收案與劑量遞增持續推進，我們現在將從提供細部更新，轉為在 2026 年下半年報告初步安全性數據。

And I'll now turn the presentation back to Jason.

接下來我把簡報交回給 Jason。

Thanks, Barb. And also a big thank you to Dr. Hurvitz for joining us today to share her views. At ALX, we're advancing two novel cancer treatments with key near-term catalysts that have the potential to be both best-in-class and first-in-class and change care. And with this new data today, we have now demonstrated in two studies in two HER2-positive cancers that EVO is a very active drug and that a CD47 targeted approach can drive transformational benefit to patients.

謝謝你，Barb。也非常感謝 Hurvitz 醫師今天加入我們並分享她的觀點。在 ALX，我們正推進兩項新穎的癌症治療，近期有關鍵催化劑（catalysts），有潛力同時成為同類最佳（best-in-class）與首創同類（first-in-class），並改變照護模式。而透過今天的新數據，我們已在兩項研究、兩種 HER2 陽性癌症中證明 EVO 是一個非常活躍的藥物，且以 CD47 為標的的方法能為患者帶來具變革性的效益。

And again, although not the focus for today, we remain as excited about the potential of our EGFR-targeted ADC, which is also progressing quite well. We now have a stronger balance sheet to fully execute through key milestones over the next year to two years, and this really sets us up well for further execution and further catalysts.

此外，雖然這不是今天的重點，我們對於以 EGFR 為標的的 ADC 潛力仍同樣感到振奮，且其進展也相當順利。我們現在擁有更強健的資產負債表，足以在未來一到兩年內完整執行關鍵里程碑，這也讓我們能更好地持續推進執行並迎接後續催化劑。

In sum, Q1 was a strong quarter for us in terms of new data, new leadership within our team and a new financing. So the message for today is one of building momentum as our conviction in both programs remains high, and we're looking forward to additional updates very soon.

總結而言，第一季對我們來說是強勁的一季，包含新數據、團隊內的新領導，以及新的融資。因此今天要傳達的訊息是：隨著我們對兩個計畫的信心依然高昂，我們正在累積動能，並期待很快帶來更多更新。

With that, I'll turn the call back over to the operator for questions. And again, thanks again for the time this morning.

接下來我把電話會議交回給接線員進行提問。也再次感謝各位今天早上的時間。

(Operator Instructions) Kaiyue Yang, UBS Securities.

（接線員指示）UBS Securities 的 Kaiyue Yang。

Congrats on the updates and progress. This is Kaiyue Yang for Michael Yee from UBS. Two for us. The first question for management. So congrats on the data today. So for your upcoming interim data readout in mid-2027 from your ongoing Phase II ASTENBreast study, what would you say is compelling results in terms of ORR and also DOR? And do you plan to put out data on mPFS?

恭喜你們的更新與進展。我是 UBS 的 Kaiyue Yang，代替 Michael Yee 提問。我們有兩個問題。第一個問題給管理團隊。再次恭喜今天的數據。針對你們正在進行的第二期 ASTENBreast 研究，預計於 2027 年年中公布期中數據；就 ORR 與 DOR 而言，你們認為什麼樣的結果算是具吸引力？另外，你們是否計畫公布 mPFS 的數據？

And what would be good data for mPFS? The second question for Dr. Hurvitz, could you please help us understand how do you plan to use this drug in the clinical setting if this is approved? Do you expect to test everybody for CD47 expression?

那麼，對 mPFS 而言，什麼樣的數據會是好的？第二個問題給 Hurvitz 醫師：若此藥獲得核准，請協助我們理解你會如何在臨床上使用這個藥物？你是否預期會對所有人檢測 CD47 表現？

Great. Thanks, Kyle. Appreciate the question. So yes, on the first one, and I'll let Barb weigh in as well. I think we've been very pleased with enrollment to date on our breast study. It's going quite well. Certainly, this data, which we've been able to share just over the last couple of months with the investigators has furthered that enthusiasm.

好的。謝謝你，Kyle。感謝你的提問。是的，關於第一個問題，我也會請 Barb 一起補充。我想我們對目前乳癌研究的收案進度感到非常滿意。進展相當順利。當然，這些數據——我們在過去幾個月才剛能與研究者分享——也進一步提升了大家的熱情。

So I think as Barb highlighted well in her comments, feel very good about our time lines and delivering really meaningful data mid-'27. But Barb, do you want to weigh in more on just what we hope in terms of durability and PFS at that time?

因此我認為如 Barb 在評論中所強調的，我們對時程非常有信心，並可在 2027 年年中交付真正具意義的數據。不過 Barb，你是否想再多談一些，關於到那個時間點我們對持久性與 PFS 的期待？

Yes, absolutely. Well, as Dr. Hurvitz said, most of the available therapies are not producing very good outcomes for patients after ENHERTU. Much of the data suggests that the response rate may be 15% if you were to receive a trastuzumab chemotherapy treatment alone without evorpacept. So a 30% response rate would be a doubling of what we would expect to see without the evorpacept.

是的，絕對是。嗯，正如 Hurvitz 醫師所說，在 ENHERTU 之後，多數現有可用的治療對病患的療效並不理想。許多數據顯示，如果你只接受曲妥珠單抗合併化療、而不加入 evorpacept，反應率可能約為 15%。因此，30% 的反應率將是我們在沒有 evorpacept 情況下預期的兩倍。

So I think anything north of 30% would be a very, very good outcome with a duration of 6 months plus. As you've seen in the data that we reported previously, one of the things that's so compelling about evorpacept is that when we see a response, we see a very good duration of response. By middle of 2027, I think the duration of response will be pretty preliminary.

所以我認為任何高於 30% 的結果，且反應持續時間達 6 個月以上，都會是非常、非常好的成果。正如你們在我們先前公布的數據中所看到的，evorpacept 之所以如此引人注目的一點是，一旦出現反應，我們會看到非常好的反應持續時間。到 2027 年年中，我認為反應持續時間的數據仍會相當初步。

So I'm expecting that with 80 patients worth of data that we can assess response rate pretty well. Duration of response may be somewhat truncated, but I would hope to see somewhere in the range of 6 months plus with immature data. And I would think that PFS might be too immature to report, but it really depends on the continued progress. So we'll have to see.

因此我預期，累積到 80 位病患的數據後，我們可以相當好地評估反應率。反應持續時間可能會有些被截短，但我希望在數據尚未成熟的情況下，仍能看到約 6 個月以上的區間。而我認為 PFS 可能還太不成熟而無法報告，但這真的取決於後續進展。所以我們還得再看看。

Yes. And Dr. Hurvitz, whether you have comments on your expectations for the ASPEN-09 data or in particular, the second part of the question about the role of CD47 testing in the clinical practice if evorpacept is able to get to market.

是的。Hurvitz 醫師，想請問您是否能就您對 ASPEN-09 數據的期待發表看法，或特別是問題的第二部分：若 evorpacept 能夠上市，CD47 檢測在臨床實務中的角色會是什麼？

Yes. Thank you, Barb. I fully agree with your -- what you stated about the ASPEN-09 study. I mean I think seeing anything around 30% objective response rate and a PFS of six months would be pretty important in patients that heavily pretreated. So I echo your comments. In terms of the additional question regarding how we would use CD47 expression, I think this is something that's really very compelling and interesting.

是的。謝謝你，Barb。我完全同意你——你對 ASPEN-09 研究所說的內容。我的意思是，我認為在這些接受過大量前線治療的病患中，若能看到約 30% 的客觀反應率，以及 6 個月的 PFS，將會相當重要。所以我呼應你的評論。至於額外的問題，也就是我們會如何使用 CD47 表現量，我認為這確實非常有吸引力且很有意思。

And the ASPEN-09 study is going to allow patients, as Barb stated, with both CD47 low and high tumor expression so that we can validate these data. We have to keep in mind, it was a small number of patients, but the data were really pretty interesting and compelling. So if CD47 is validated as being a predictive marker for benefit from evorpacept, then I do think we will be probably seeing it developed as a companion diagnostic.

而 ASPEN-09 研究將允許如 Barb 所說、同時納入 CD47 低與高腫瘤表現的病患，讓我們能夠驗證這些數據。我們必須記住，樣本數很小，但數據確實相當有趣且具說服力。因此，如果 CD47 被驗證為可預測 evorpacept 獲益的標記，我確實認為我們很可能會看到它被開發為伴隨診斷。

But it's too little data at this point to see -- to make that statement definitively that that's how we'll be doing -- using it. I've been treating breast cancer patients for over 20 years. And the data with ENHERTU were really exciting when we first saw them come out in 2019. I feel that same flurry of excitement seeing these data because it's pretty tough to treat patients post T-DXd now.

但目前數據仍然太少，還不足以——做出明確結論說我們將會——如何使用它。我治療乳癌病患已超過 20 年。2019 年我們首次看到 ENHERTU 的數據時，真的非常令人振奮。現在看到這些數據，我也有同樣一陣興奮感，因為在 T-DXd 之後要治療病患確實相當困難。

Their progression-free survival, their duration of response to the next line of therapy is pretty short. And so these data provide patients a lot of hope. So I'm excited to see the data validated just taking into consideration that it is a small number of patients.

他們的無惡化存活期，以及對下一線治療的反應持續時間，都相當短。因此，這些數據為病患帶來了很大的希望。所以我很期待看到這些數據被驗證，同時也要考量到目前病患數仍然不多。

Derek Archila, Wells Fargo.

Wells Fargo 的 Derek Archila。

Congrats on the update here. Just a few questions from us. I think, first, you alluded in the prepared remarks, but just remind us the population in ASPEN-09 and then how it compares to some of the patients from the update today, that would be helpful. And then just two quick ones. So I think you mentioned the 20,000 patients CD47 high post HER2. So does that assume greater than 20% CD47 expression?

恭喜這次更新。我們這邊有幾個問題。我想首先，你們在事先準備的講稿中有提到，但請再提醒我們 ASPEN-09 的受試族群是什麼，以及它與今天更新中部分病患相比如何，這會很有幫助。接著還有兩個簡短問題。我想你們提到在 HER2 後線、CD47 高表現的病患有 20,000 人。所以這是以 CD47 表現量大於 20% 為假設嗎？

Or I just want to make sure the cutoff is the same? And then with the data here and the proof of concept with the zani combo, I guess, how do you think about further developing this?

還是我只是想確認，這個 cutoff（切點）是否相同？另外，基於這裡的數據以及 zani 聯合療法的概念驗證，我想請問你們如何看待後續的進一步開發？

Yes, sure. Those are great questions. Thanks, Derek. So I think in terms of the population that we're studying now, it is this population. That's what I think really derisk, if you will, this current study. I think as we walk through today, this is a late-line breast population. 100% of the patients in this cohort had seen prior in HER2. On average, it's seen five prior lines of HER2-directed therapy, et cetera.

是的，當然。這些都是很好的問題。謝謝你，Derek。我想就我們目前研究的族群而言，就是這個族群。我認為這在某種程度上（如果你願意這麼說）降低了這項目前研究的風險。正如我們今天所說明的，這是一個後線乳癌族群。這個隊列中 100% 的病患都曾接受過 HER2 的既往治療。平均而言，病患先前接受過 5 線 HER2 標靶治療等等。

So I think the beauty of this design that we're pursuing now is it's effectively the same. So I do think that definitely contributes to our confidence in this study. Then on the second question, and I can have Barb weigh in on this. I think we do know from the literature, we expect that the expression profiles will be different across different tumor types.

所以我認為我們現在採用的這個設計之美在於，它基本上是相同的。因此我確實認為，這明顯提升了我們對這項研究的信心。至於第二個問題，我也可以請 Barb 補充。我想我們從文獻中確實知道，不同腫瘤類型之間的表現譜預期會有所不同。

That's certainly what we've seen when we look at breast and gastric. But again, I think what's so encouraging is that there's just a lot of room here in terms of choosing a cutoff, if you will. So Barb, do you want to speak to that a little more?

這當然也是我們在比較乳癌與胃癌時所看到的。但我認為令人鼓舞的是，在選擇切點方面仍有很大的空間。Barb，你要不要再多談一點？

Yes. I think one of the most important things about what we will understand with the data from ASPEN-09 is what's the optimal cut point? Where on the total membrane staining scale, would we see the greatest differential between high response rate in the CD47 positive versus CD47 low. And it's likely to be a continuum, and we're likely to be able to not see a cliff where it's crystal clear.

好的。我認為，從 ASPEN-09 的數據中我們將理解的最重要事情之一，就是最佳切點是什麼？在總膜染色（total membrane staining）的量表上，在哪個位置我們會看到 CD47 陽性相較於 CD47 低表現之間，反應率差異最大？而這很可能是一個連續光譜，我們也很可能看不到一個非常清楚、像斷崖般的界線。

What we've seen in both the gastric and the breast study, though, is we're seeing about half of patients overexpress CD47. At least in our gastric study with a larger sample size, we shared at SITC in the fall of 2025, a variety of different cut points that range from 45% to 57%. Gastric may be different than breast, though. And so with the Zani data, we have just such a small number of patients.

不過，我們在胃癌與乳癌研究中看到的是，大約有一半的病患 CD47 過度表現。至少在我們樣本數較大的胃癌研究中，我們在 2025 年秋季的 SITC 上分享了多種不同的切點，範圍約在 45% 到 57%。但胃癌可能與乳癌不同。而就 Zani 的數據而言，我們的病患數非常少。

So -- but what we saw in the Zani trial, again, about 50% were CD47 high. One of the biggest reasons we increased the sample size from 80 to 100 is just so that we could get more data because this point exactly what is the cut point? How does it differentiate response rates? And what does it do to the population in terms of potential commercial opportunity balanced against finding the best treatment effect for patients is a really important question.

所以——但我們在 Zani 試驗中看到的同樣是，約 50% 為 CD47 高表現。我們把樣本數從 80 增加到 100 的最大原因之一，就是為了取得更多數據，因為正如你指出的這個點：切點到底是什麼？它如何區分反應率？以及它對族群規模的影響——就潛在商業機會而言——如何在為病患找到最佳治療效果之間取得平衡，這是一個非常重要的問題。

So ASPEN-09 will help us optimize the cut point. My best guess today is it will be somewhere in the range of 50%, 60%, 70% of patients could be CD47 overexpressing, but we'll see. What also, of course, are the two slides that Dr. Hurvitz showed where the rates are higher in patients who have more advanced disease. They are higher in the cell lines post ENHERTU, and they are higher in patients who are HER2 positive. So it could even be higher than 50%. We'll learn a lot from the ASPEN-09 on that exact question.

因此 ASPEN-09 將幫助我們最佳化切點。我目前最好的猜測是，可能會落在約 50%、60%、70% 的病患可能屬於 CD47 過度表現，但我們會再看。當然，Hurvitz 醫師展示的那兩張投影片也顯示，在疾病更晚期的病患中，比例更高。在 ENHERTU 後的細胞株中更高，在 HER2 陽性的病患中也更高。所以甚至可能高於 50%。我們會從 ASPEN-09 中在這個精確問題上學到很多。

And I think your last question, Derek, just on zani, a couple of comments there. I think, one, really pleased with the partnership with Jazz and what we're seeing here for patients. I think no question that very strong activity with this combination. The second thing, and I think why it's important to look back at our mechanism is EVO works in combination with an Fc active antibody, and it was designed to do so.

我想你最後一個問題，Derek，關於 zani，我這裡有幾點評論。第一，我們對與 Jazz 的合作以及我們在病患身上看到的結果感到非常滿意。我認為毫無疑問，這個組合展現出非常強勁的活性。第二點，我認為之所以重要的是回頭看我們的作用機制：EVO 是與一個具 Fc 活性的抗體聯合使用而發揮作用，而且它就是為此而設計的。

And so I think what's really promising about the totality of the data is whether we're combining EVO with traz, with zani, with Rituxan, with an anti-CD38 like Sarclisa, we see activity. And I think that's right on mechanism. And so for us, taking the combination of Evo plus traz going forward makes sense. Again, it's the exact same combination that we utilized in our ASPEN-6 study, which is a randomized study, as you know. So I do think that gives us a lot of conviction here going forward.

因此，我認為整體數據最令人振奮之處在於：無論我們把 EVO 與 traz、與 zani、與 Rituxan、或與像 Sarclisa 這樣的抗 CD38 藥物合併，我們都看到活性。我認為這完全符合其作用機制。因此，對我們而言，未來推進 Evo 加 traz 的組合是合理的。同樣地，這正是我們在 ASPEN-6 研究中使用的完全相同的組合；如你所知，那是一項隨機研究。所以我確實認為，這讓我們對後續推進有很強的信心。

Ashleigh Acker, Piper Sandler.

Ashleigh Acker，Piper Sandler。

This is Ashleigh on for Ally. Just two questions from us. So just curious to learn what's the latest on the companion diagnostic development. I know you guys have talked about this on previous earnings calls. So just looking for some updated thoughts there. And also just based on the data today and this data set, it looks like the CD47 biomarker strategy is being further validated. So does this impact the statistical powering at all for ASPEN-09?

我是 Ashleigh，代 Ally 提問。我們有兩個問題。首先想了解一下伴隨診斷（companion diagnostic）的開發最新進展。我知道你們在之前的財報電話會議中談過這件事。所以想聽聽你們目前更新的看法。另外，基於今天的數據以及這組資料，看起來 CD47 生物標誌物策略正在進一步被驗證。那這是否會影響 ASPEN-09 的統計把握度（statistical powering）？

Sure. That's great question. Do you want to go on the CDx front, Barb?

當然。這是個很好的問題。Barb，你要先談談 CDx 這一塊嗎？

Yes. Sorry, Jason. Yes, the Ventana Laboratory is our partner. We are working right now on developing a companion diagnostic. What we want is by the time we are finishing the full data set of ASPEN-09, as I alluded to earlier, setting a cut point that could then be available for preselection of patients potentially in a Phase III trial. That's our base case assumption is that our Phase III would be in preselected patients.

好的。抱歉，Jason。是的，Ventana 實驗室是我們的合作夥伴。我們目前正在開發伴隨診斷。我們希望在完成 ASPEN-09 的完整數據集時（如我先前提到的），能設定一個切點（cut point），以便在第三期試驗中可能用於預先篩選病患。我們的基本情境假設是：我們的第三期試驗將在預先篩選的病患中進行。

So we will have an assay available. And then if that Phase III study is positive, of course, then we would work with our Ventana partner to not only bring evorpacept to market, but to ensure that the companion diagnostic were then commercially available. In terms of statistical powering -- go ahead. Go ahead, Jason.

因此我們會有一個可用的檢測方法（assay）。接著如果該第三期研究結果為正，當然我們會與 Ventana 合作夥伴一起，不僅將 evorpacept 推向市場，也確保伴隨診斷在商業上可取得。至於統計把握度——請繼續。Jason，你先。

No, go ahead, Barb. I just -- I mean, to kick that off, I mean, I think, of course, we're not going to power the study at 100% ORR, and that's not what we're going to do. And I think -- but if you look at the beauty of a targeted approach, I think it allows and our hope is it will allow a much more targeted Phase III where we can run a tighter registrational study with assumptions that I think are reflective of what we've seen, which has been a really strong spread, if you will, both in terms of ORR as well as DOR and PFS. But go ahead,

不，你先說，Barb。我只是——我的意思是，先起個頭：當然，我們不會把研究設計成以 100% ORR（客觀緩解率）來做把握度計算，這不是我們要做的。而且我認為——但如果你看標靶式方法的優點，我認為它能夠、也希望能夠讓我們做一個更聚焦的第三期試驗，讓我們以更緊湊的註冊性研究（registrational study）來進行，並採用我認為能反映我們所見結果的假設；我們看到的是非常強的差異表現（spread），不論是在 ORR、DOR（緩解持續時間）以及 PFS（無惡化存活期）方面。但你繼續，

Barb, I know I cut you off there.

Barb，我知道我剛剛打斷你了。

No, no, that's exactly right. I think with a single-arm trial, ASPEN-09, the statistics are really around estimating the point estimate of the response rate and narrowing the confidence intervals with a larger sample size. But what ASPEN-09 does is it allows us potentially greater precision with this larger trial of 120 patients such that we can then have a lot of confidence walking into a Phase III subsequently and really understanding the treatment effect in patients based on their CD47 status.

不不，你說得完全正確。我認為在單臂試驗 ASPEN-09 中，統計主要是圍繞估計反應率的點估計值，並透過更大的樣本數來縮小信賴區間。但 ASPEN-09 的作用在於：透過這項較大的試驗（120 位病患），讓我們可能獲得更高的精確度，如此我們之後進入第三期時就能非常有信心，並真正理解在不同 CD47 狀態病患中的治療效果。

Daniel Bronder, Cantor.

Daniel Bronder，Cantor。

This is Daniel Bronder on for Li Watsek. We have a couple, one more technical and then one regulatory. We'll start with the technical one. On the poster from ESMO breast, you have the concordance of HER2 amplification by ctDNA and FISH. I was just curious how that translates into HER2 positivity in IHC. And then on the regulatory front, you mentioned registrational trials a few times in your opening remarks and in the previous response as well. Does that mean you're ruling out a potential accelerated approval based on ASPEN-09? Or are you keeping optionality here?

我是 Daniel Bronder，代 Li Watsek 提問。我們有幾個問題，一個偏技術面，另一個偏法規面。先從技術面開始。在 ESMO 乳癌的海報中，你們展示了以 ctDNA 與 FISH 檢測 HER2 擴增的一致性。我想了解這如何轉換到 IHC 的 HER2 陽性判定。另外在法規面，你們在開場發言以及前一個回覆中多次提到註冊性試驗。這是否表示你們排除了基於 ASPEN-09 申請加速核准（accelerated approval）的可能性？還是你們仍保留彈性？

Those are great questions. Go ahead.

這些都是很好的問題。請繼續。

I'm sorry, I should stop doing that. And Dr. Hurvitz, I'll have you make some comments after I'll address the regulatory one first, give you a chance, but I'll have you talk a little bit to the HER2 data that was in the poster. So the regulatory strategy, Jason said a few minutes ago that we do not have an expectation that we could replicate 100% response rate. That would be fabulous if we could.

抱歉，我不該一直這樣。Hurvitz 醫師，我會在我先回答法規問題後請你補充一些看法，讓你有機會談談海報中的 HER2 數據。所以在法規策略方面，Jason 幾分鐘前提到，我們不預期能複製 100% 的反應率。如果能做到那會非常棒。

And if we do, I think absolutely, we would talk to the health authorities, US FDA about an accelerated approval strategy. I just think that, that is such a high bar, and we're also very, very aware that an advantage for patients would be anything north of, say, 30%. So we'll just have to wait and see what those response rate -- what the response rate is in ASPEN-09.

如果真的做到，我認為我們絕對會與主管機關、也就是美國 FDA 討論加速核准策略。我只是認為那個門檻非常高；同時我們也非常清楚，對病患而言，任何高於例如 30% 的結果都會是優勢。所以我們只能等待並觀察 ASPEN-09 的反應率——也就是 ASPEN-09 的反應率會是多少。

I think regulatory approvals for single-arm trials when you have a combination of two agents, very difficult to get an accelerated approval. It's also true that it's very difficult to get an accelerated approval with retrospective application of a companion diagnostic. We would need at least some additional prospectively selected patients. So there are a lot of regulatory considerations.

我認為在單臂試驗中、且是兩種藥物的聯合治療，要取得加速核准非常困難。同樣地，若要以回溯方式（retrospective）套用伴隨診斷來取得加速核准也非常困難。我們至少需要一些額外、前瞻性篩選（prospectively selected）的病患。因此有許多法規層面的考量。

But I think at this case, that is not our base case. Our base case is that a Phase III trial will be required because the bar is high for accelerated approval, but we'll just have to wait and see what the response rate is. If it's extraordinary, we'll talk about it. If it's somewhere north of 30%, but less than 100%, it's going to be an uphill battle. But obviously, that would benefit patients if we could bring it to market sooner, but we'll wait and see. So maybe I'll flip it back to Dr. Hurvitz to talk a little bit about some of this HER2 data in the poster.

但我認為在這個情況下，那不是我們的基本情境。我們的基本情境是需要一項第三期試驗，因為加速核准的門檻很高；不過我們仍要等著看反應率是多少。如果結果非常卓越，我們會去討論。如果反應率高於 30% 但低於 100%，那將會是一場艱難的攻堅。但顯然，如果我們能更早把藥物推向市場，病患會受益；不過我們會先觀察結果再說。所以我把問題交回給 Hurvitz 醫師，請你談談海報中的一些 HER2 數據。

Yes. Thank you, Barb. The HER2 data is actually kind of interesting. So there are 2 aspects. First, there was a difference in the central confirmation of HER2-positive disease that was shown in the poster where 10 of the patients out of the 24 were noted to have centrally confirmed HER2-positive disease and 14 were not. And I would just call out that this is not uncommon. It's been reported in other studies that there is discordance.

好的。謝謝你，Barb。HER2 的數據其實有點有趣。所以有兩個面向。第一，在海報中顯示的 HER2 陽性疾病中央確認（central confirmation）結果存在差異：24 位病患中有 10 位被判定為中央確認的 HER2 陽性，而 14 位則不是。我想特別指出，這並不少見。其他研究也曾報告存在不一致（discordance）。

And it may not necessarily mean that there's been HER2 loss that's occurred over time. It may actually be related to artifact from testing older tissue. It's important to keep in mind that in order for patients to enroll in the study, HER2 status was based on archival tissue that was read locally. But once they got on the study, the assays that were done were done on fresh biopsy samples obtained at the start of the study from most patients, and those were tested centrally.

而且這未必一定代表隨著時間推移發生了 HER2 流失（HER2 loss）。這實際上可能與檢測較舊組織所造成的偽影（artifact）有關。需要記住的是，為了讓患者能夠入組研究，HER2 狀態是依據由當地判讀的存檔組織（archival tissue）。但一旦進入研究後，所進行的檢測多數是在研究開始時取得的新鮮活檢樣本上完成，且由中央實驗室進行檢測。

And so the testing changed from local to central and also from archival tissue to fresh tissue after in HER2 for the vast majority of subjects. So either of those factors could have contributed to the differences between local HER2 positive results and central positive results. Another point was in the poster in Table 2, there were some data presented looking at concordance between HER2 amplification status by the central tissue-based FISH as well as plasma ctDNA next-generation sequencing.

因此，對於絕大多數受試者而言，HER2 的檢測從當地改為中央，且也從存檔組織改為研究開始後的新鮮組織。所以，這兩個因素中的任何一個都可能導致當地 HER2 陽性結果與中央陽性結果之間的差異。另一點是，在海報的表 2 中，呈現了一些資料，用以觀察中央以組織為基礎的 FISH 所測得的 HER2 擴增狀態，以及血漿 ctDNA 次世代定序之間的一致性。

And it's important to call out that of the six patients with HER2 amplification by FISH -- or excuse me, the seven patients, six of them were also noted to have amplification by ctDNA. Just one of the patients there did not, and that may have just been due to the fact that there wasn't enough circulating. There was a low tumor fraction. It was below the threshold of expression.

值得特別指出的是，在以 FISH 檢出 HER2 擴增的 6 位患者——抱歉，是 7 位患者中，有 6 位也被 ctDNA 檢出擴增。其中只有 1 位沒有，這可能只是因為循環中的量不夠。腫瘤分率（tumor fraction）偏低。低於表現量的門檻。

But those that were negative centrally by FISH were also negative by ctDNA. And so that's reassuring and provides sort of validation that the central HER2 amplification is correlating well with circulating tumor DNA.

但那些在中央以 FISH 判定為陰性的，也同樣在 ctDNA 上為陰性。因此這令人安心，並提供某種程度的驗證：中央的 HER2 擴增結果與循環腫瘤 DNA 之間具有良好的相關性。

Roger Songm, Jefferies.

Roger Songm，Jefferies。

Congrats on the positive data and excited about the momentum going into ASPEN-09. Maybe two from us. So you previously mentioned we're seeing roughly half of HER2-positive patients being CD47 high. As we're into the early ASPEN-09 screening, is the observations you're seeing consistent with that half of HER2-positive patients being CD47 high? And then is tissue adequacy and turnaround time any potential gating factor here for enrollment?

恭喜正向數據，也很期待進入 ASPEN-09 的動能。我們這邊可能有兩個問題。你先前提到，我們看到大約一半的 HER2 陽性患者屬於 CD47 高表現。在 ASPEN-09 早期篩選階段，你們目前觀察到的情況是否與「約一半 HER2 陽性患者為 CD47 高」一致？另外，組織樣本是否足夠以及檢測回報時間，會不會成為入組的任何限制因素？

Yes, sure. Good question. So I think on the ASPEN-09 front, of course, we're going to monitor that closely. And then in terms of the disclosure, we'll wait and disclose that when we get to the data readout on 80 patients. Obviously, I think it's something that's important, and we're able to monitor really quite quickly. So the lag has not been a concern. And of course, I think our team is focused on that. But Barb, do you want to add anything there?

是的，當然。好問題。我想在 ASPEN-09 方面，我們當然會密切監測。至於揭露，我們會等到 80 位患者的數據讀出時再行披露。顯然我認為這很重要，而且我們能夠非常快速地進行監測。所以目前延遲並不是問題。當然，我們團隊也專注在這件事上。不過 Barb，你要不要補充？

Only that the ASPEN-09 study enrolls patients irrespective of CD47. So there is no urgency in terms of the turnaround. You're absolutely right that it would be something that we need to ensure that we work through those processes for a future Phase III, assuming that, that future Phase III requires CD47 overexpression for entry. But this study does not. So the urgency is not there. But as Jason says, we're not going to disclose prevalence rates or any of the biomarker data until we come out with data in the middle of 2027.

我只補充一點：ASPEN-09 研究是不論 CD47 狀態皆可入組。因此在回報時程方面並沒有急迫性。你說得完全正確：若未來進入第三期（Phase III），且假設該第三期需要 CD47 過度表現作為入組條件，那我們就必須確保把這些流程跑順。但本研究並不需要。所以沒有那種急迫性。不過如 Jason 所說，在 2027 年年中公布數據之前，我們不會披露盛行率或任何生物標記資料。

Oliver McCammon, LifeSci Capital.

Oliver McCammon，LifeSci Capital。

This is Oliver McCammon on for Sam Slutsky. So in the Phase Ib/II breast cancer study, you defined CD47 high as total membrane staining of 20% or greater. And in the past, you talked about 10% or greater IHC 3+ as being a cutoff for CD47 high. Can you just discuss the nuances of the two cutoffs used and the selection process?

我是 Oliver McCammon，代 Sam Slutsky 提問。在 Ib/II 期乳癌研究中，你們將 CD47 高表現定義為總膜染色（total membrane staining）達 20% 或以上。而過去你們談到以 IHC 3+ 達 10% 或以上作為 CD47 高表現的切點。能否請你們說明這兩種切點使用上的細微差異，以及選擇流程？

Sure. Thanks, Oliver. Again, I think Barb hit on this, but we fully anticipated even ahead of this data that the expression profiles would be different. There's, of course, a lot of similarities between HER2 positive tumor types. Insofar as typically a drug that works in one will work in the other. That said, I think there will be a difference in expression, and we're seeing that here.

當然可以。謝謝你，Oliver。我想 Barb 也提到過，但即使在這些數據出來之前，我們就完全預期表現型（expression profiles）會有所不同。當然，HER2 陽性腫瘤類型之間有很多相似之處。就某種程度而言，通常一個腫瘤類型有效的藥物，在另一個也會有效。但我認為表現量仍會有差異，而我們在這裡也確實看到了。

And again, I would just highlight that if you think about defining a cutoff when you see ORR as high as we're seeing across both of those studies, it suggests there's probably many different right answers, if you will, in terms of the cutoff we could use. But Barb, do you want to expand on that?

另外我也想強調：當你看到兩項研究的 ORR 都像我們看到的那麼高時，若要去定義一個切點，這表示在切點選擇上可能有很多種「都對」的答案。不過 Barb，你要不要再延伸說明？

Just in terms of total membrane staining and how that's calculated. So the proportion of cells that are one plus are multiplied by one, the proportion of cells that are two plus IHC stain staining intensity would be multiplied by two and so forth. So IHC 3, multiply the proportion of cells that are IHC 3+ by -- and then you add those. So it's a cumulative total.

我補充一下總膜染色以及其計算方式。也就是：IHC 染色強度為 1+ 的細胞比例乘以 1；2+ 的細胞比例乘以 2；以此類推。所以 IHC 3+ 就是把 IHC 3+ 的細胞比例乘以 3——然後把這些加總。因此它是一個累積總分。

So if I were to look at the threshold for gastric 10% or more of cells being three plus, that would potentially be about a score of 30. It may be that different labs and slightly different methods. But to put it in context, it's similar, but it's -- cut point was a little bit lower in the zanidatamab trial. It was zanidatamab-evorpacept was a very small trial. So we will look again once we have data from ASPEN-09 and optimize that.

所以如果我看胃癌的門檻：3+ 細胞比例達 10% 或以上，那可能相當於大約 30 分。不同實驗室與略有差異的方法可能會有影響。但放在脈絡中看，它是相近的，只是——在 zanidatamab 試驗中的切點稍微低一些。zanidatamab-evorpacept 是一個非常小型的試驗。因此，等我們拿到 ASPEN-09 的數據後，會再重新檢視並加以最佳化。

So it may change. In fact, that likely change much, much sample size, but technically we are doing it. And we modified it a bit once we start work towards development (technical difficulty) with our partners at (technical difficulty).

所以它可能會改變。事實上，隨著樣本數大幅增加，這很可能會改變，但在技術上我們確實正在進行。而且當我們開始與合作夥伴推進開發工作時，我們也稍微做了調整（技術問題）與我們的合作夥伴在（技術問題）。

This now concludes our question-and-answer session. I would like to turn the floor back over to Jason Lettmann for closing comments.

現在問答環節到此結束。我想把時間交回給 Jason Lettmann 作結語。

Great. Thanks, everybody. It was a strong quarter for us. I appreciate all the engagement here today. Both programs, as we mentioned, are on track and super excited about what we're seeing in both. So again, I appreciate the questions and support and looking forward to future updates. Enjoy your Friday and your weekend. Thanks so much.

很好。謝謝各位。對我們而言這是一個表現強勁的季度。我很感謝今天大家的踴躍參與。如我們提到的，兩個項目都按計畫推進，我們也對兩者所看到的結果感到非常振奮。再次感謝大家的提問與支持，期待未來的更新。祝各位週五與週末愉快。非常感謝。

Ladies and gentlemen, thank you for your participation. This does conclude today's teleconference. You may disconnect your lines, and have a wonderful day.

各位女士先生，感謝您的參與。今天的電話會議到此結束。您可以掛斷電話，祝您有美好的一天。